11The Life Course

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Some racial and ethnic health differences are consistent across the age range, appearing among younger as well as older people. This consistency suggests that early life conditions could be important for late-life differences and that understanding the relative health status of racial and ethnic groups in late life may require study of health factors, including all the factors just discussed, at younger ages. The empirical evidence that late-life differences develop from events at earlier ages is scattered and uneven. Some evidence is indeed fairly strong, but much of it is largely suggestive and requires further confirmation.

Depending on the severity of their effects on health, early life events could produce later differences in three ways. First, if these events lead to some risk of early death, it could affect the eventual composition of cohorts of the aged of different racial and ethnic groups. The survivors in each group may be selected in different ways, producing differences in health status. Such selection processes are discussed above; to fully understand them would require a comprehensive investigation of the life course, beginning at the earliest ages.

Second, early life events may impair health, or alternatively lead to more robust health, and so confer permanent disadvantages or advantages or possibly a chronic risk of illness. Injuries that produce permanent disability, for instance, obviously have lifetime implications. Illness or malnutrition may affect the normal physiology and functioning of vital organs in a permanent way. If the immediate health effects are reversible, they may still leave someone more susceptible to later illness. For instance, impaired fetal development of the respiratory system could lead to greater susceptibility to chronic obstructive respiratory disease (Ben-Shlomo and Kuh, 2002).

Third, early life events may somehow set one on a pathway that results, possibly many years later, in impaired—or enhanced—health (Hertzman, 2004). Such experiences as early schooling may not immediately affect health but may decisively influence one's eventual level of completed education and foreclose certain career paths, affecting experiences and later behavior in ways that eventually affect health. For instance, nutritional deficiencies related to poverty, even if they have no irreversible health effect, may produce lung function deficiencies that in the long run result in greater susceptibility to infections of the upper respiratory system. Pathways may involve cumulative effects but are not determinate, since health and development are subject to many influences. The plasticity of these relations means that a person's late-life health status is not certain but depends on numerous contingencies (Rutter, 1996).


Health in early life differs among racial and ethnic groups. Time trends since 1950 in birthweight and infant mortality—two basic though not necessarily the most appropriate indicators (Barker, 1998)—show consistent differences that favor whites over blacks and American Indians and Alaska Natives. For Asians and Hispanics, the contrasts with whites are less consistent, but they indicate that these minorities fare better with respect to birthweight though not, in the case of Hispanics, infant mortality. Little is known, however, about racial and ethnic differences in exposure to and experience with illnesses in early life.

Do the early life health differences that are known account for some portion of health and mortality differences among racial and ethnic groups at older ages? Although no coherent body of research attempts to assess such influences in comparison with contemporaneous or other explanations of differences, there is important research on the mechanisms by which early life environments may affect later health.

Conditions in utero and during the first year of life modify patterns of brain tissue growth and thereby alter the functioning of one or more neurophysiological centers of hormonal balance and activation. This functioning influences cellular growth, tissue development, and the ultimate physiological status and functioning of key organs, such as the heart, lungs, and kidneys. Ultimately affected are immune status, resilience, frailty, individual choices, and behavior (Hertzman et al., 2002). That early life health status has such long-term effects is demonstrated in some studies (Barker, 1998; BenShlomo and Smith, 1991), though not all (Christensen et al., 1995; Leon, 1995; Vagero and Leon, 1994).

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. Some research has focused directly on the effects of early childhood status and deprivation on late adult health and mortality (Ben-Shlomo and Kuh, 1997; Ben-Shlomo and Smith, 1991; Blackwell et al., 2000; Felitti et al., 1998; Forsdahl, 1978, 2002; Hayward and Gorman, 2002; Moore et al., 1997; Power et al., 1990, 1998; Rahkonen et al., 1997; Wadsworth, 1991; Wadsworth and Kuh, 1997). Few such studies focus on ethnic and racial differences in the processes involved (Doblhammer, 2002; Warner and Hayward, 2002). Few studies also attempt to identify mediating mechanisms, which are important because low socioeconomic status is not itself a disease nor intrinsically tied to poorer health.

One possible mediating mechanism is access to and use of health care. Differences in health care between white and minority children and their mothers have been documented (Institute of Medicine, 2002). This may be relevant to late-life health status and mortality, though the effects of prenatal care on fetal growth and birthweight are now in dispute. The relevance of other aspects of health care—less use of prescribed medications, fewer visits to physicians, poorer compliance with vaccination schedules—has not been confirmed.

Another mediating mechanism, much more complex and virtually unexplored, involves the mutual dependence of health and socioeconomic status (discussed earlier as a possible selection process). If impoverished early environments are associated with worse health, this may limit one's opportunities in life, which in turn may expose one to greater health risks. Health differences in adulthood could be exacerbated by such a mechanism. Some research has attempted to model the influences involved (Palloni and Milesi, 2002; Power et al., 1986), and other research has sought to determine the magnitude of the effects (Hack et al., 2002; Lundberg, 1991; Nystrom Peck, 1992; Nystrom Peck and Lundberg, 1995; Nystrom Peck and Vagero, 1987; Power et al., 1990; Wadsworth, 1986). But these efforts have met only limited success (Palloni and Milesi, 2002), and the skeptical tone of early evaluations is still appropriate today (Blane et al., 1993). The extent to which such a mechanism may account for racial and ethnic differences is unknown.

Other features of early environments that may put individuals on pathways to disadvantage include exposure to discrimination or stigmatization (as discussed above), the physical and social isolation of a group, and exposure to conflict and violence. Some research suggests that stressful events, more commonly experienced in deprived social environments, lead to poor maternal health and increase the risks of fetal underdevelopment and low birthweight (Hogue and Hargraves, 1993; Williams and Collins, 1995; Zambrana et al., 1997). Evidence from animal and human studies shows that infants subjected to abuse, lack of parental care, and, more generally, higher levels of violence and hostility experience physiological changes in hormonal regulatory mechanisms, changes that are precursors of and a predisposition to various chronic conditions (Bornstein and Cote, 2001; Coe, 1999; Francis et al., 1999; Hertzman et al., 2002). Experiencing certain environments may “mark” individuals—perhaps through a number of physiological imprinting mechanisms—in ways that could increase the risk of later morbidity.

Understanding the implications of early life events, as well as of events over the life course, may in some cases require a focus on health in late life or even at the oldest ages. People who live to extremely old ages tend to remain healthy and functional much longer than others (Hitt et al., 1999). Expanding knowledge of the extremely long-lived population holds special significance for racial and ethnic minorities. For instance, the Hispanic paradox—the better health of Hispanics relative to better-off whites (Franzini et al., 2001)—raises the question of whether there is a robust aging minority population that might reward study.


Improving understanding of the consequences of early experiences for differences in adult health and mortality is a complex task. Several interrelated types of work are needed. First, research is needed to identify key early experiences and the precise mediating mechanisms through which they affect later health. Though some important factors have been identified, more work needs to be done. Also needed is better understanding of the conditions that enhance or inhibit the effects of such factors. Second, research is needed to better document racial and ethnic differences in these early experiences. Only limited and superficial evidence on this is now available. Third, research is needed to determine whether the effects of early experiences and initial differences in them actually account for some portion of racial and ethnic differences at older ages. This issue remains unexplored.

Research Need 16: Place particular emphasis on panel studies that follow cohorts over time in order to study differences in health among racial and ethnic groups over the life course.

Such panel studies should include physiological and psychological measures as well as assessments of environmental conditions. Some such studies are in progress, following British and Canadian cohorts (Hertzman et al., 2002; Wadsworth, 1991). Other large longitudinal studies of somewhat different design, such as the National Longitudinal Survey of Youth (NLSY) and the Panel Study of Income Dynamics in the United States and a survey like the NLSY in Canada can be used for partial tests of some hypotheses. One convenient way to produce panel data might be to follow up on previously surveyed samples, such as those for other National Longitudinal Surveys, on young women, mature women, young men, and older men, even though some of the surveys have been previously discontinued. Two other longitudinal studies—the Coronary Artery Risk Development in Young Adults study and the Atherosclerosis Risk in Communities study—include, by design, samples of whites and black, and may therefore be particularly useful for looking at racial differences.

Short of cohort studies, various other approaches can be taken to analyze life course influences. Surveys of adult health could be enhanced with information about childhood experiences. Retrospective questions could be used, though they are subject to recall bias, and responses can be distorted because of current status. Data can sometimes be obtained from administrative records matched with individual survey records. For instance, birth records contain information on birthweight that could be added to a number of ongoing surveys. Similarly, school records may contain information of past illnesses or health-related events (prolonged absences, personality reports, etc.). Test scores and examination results could also be useful to roughly characterize the school environment of survey respondents. A further possible approach is to extend existing data sets by linking them with other data sources. All these approaches require interdisciplinary teams and close collaboration among funding agencies, some of which may support work on early childhood and others on adult health and mortality. There are also obviously difficult issues of methodology and data quality, problems with releasing sufficient data to allow matching, and issues of confidentiality that must be attended to in each case.

Studies could also focus on specific stages of the life course to document the operation of mechanisms that are hypothesized to mediate the effects of early experiences on adult health. If deprivation alters key physiological parameters during early childhood, it should be possible to verify this effect without a longitudinal study. Uncovering such effects is crucial to any argument that early experiences affect adult health through physiological programming or imprinting. Studies of these mechanisms may require invasive procedures (such as extensive and expensive blood tests, magnetic resonance imaging, etc.) but could be completed relatively quickly. For instance, studies could focus on metabolic variables among younger individuals exposed or not exposed to known sources of stress to determine allostatic load and to assess whether physiological plasticity of response can be lost at early ages, and, if so, with what consequences.

Studies that combine data sets covering different stages in the life course would be useful to draw inferences across life stages. With properly designed estimation (and simulation) procedures, composite data sets would allow reasonable inferences about a range of early exposure effects and about their importance relative to contemporaneous determinants of health. Besides attending to early stages in the life course, late stages might also receive some attention. Minority older adults who are exceptionally healthy might provide clues to appropriate behavior modification strategies to decrease mortality and morbidity across the lifespan. The Macarthur Successful Aging Cohort study covers whites and some blacks, but the superior health status of other racial and ethnic minorities, despite poorer socioeconomic status, suggests that they should be included in studies.

Whether implementing cohort studies or other approaches, social scientists and epidemiologists need to pay more attention to and collaborate more closely with those carrying out studies with animal models to learn about the plausible operation, boundaries, and reach of biological effects. Some of the most important work on the effects of early experiences on adult health status has been inspired by studies with monkeys and rats. Similarly, a remarkable number of studies relating early deprivation to physiological imprinting are based on animal models (Barker, 1998).