using such findings to develop effective support-based interventions for improving health across the life span.

The differential distribution of social resources across SES levels and by racial/ethnic groupings also merits additional study. So understudied and important are social processes to predisease and disease outcomes that we devote parts of three chapters to their consideration, one on personal social ties (see Chapter 5), one on the collective properties of health environments (see Chapter 6), and one on the health consequences of inequality (see Chapter 7).

Environmental stressors are known to have effects, often dramatic, across the life span. Chronic stress can precipitate insulin-dependent diabetes in animals with a genetic risk (Lehman et al., 1991), and in children stressful life events increase the symptoms of juvenile diabetes (Hagglof et al., 1991). Animals given a malignant tumor preparation and exposed to a chronic stressor (crowding) showed higher rates of malignant tumor development than those not exposed to stress (Amkraut and Solomon, 1977). Evidence like this implicates stress in predisease pathways and suggests the importance of both research designed to identify the specific mechanisms involved in these risks and the development of interventions to modify stressors that may precipitate risk conferred by genetic or behavioral vulnerability.

Adverse effects of chronic stress exposure can be seen as early as the prenatal environment. Maternal stress at 18 to 20 weeks' gestation has been found to significantly predict corticotropin-releasing hormone (CRH) at 28 to 30 weeks' gestation, even after controlling for CRH at 18 to 20 weeks (Hobel et al., 1999). Research on adult populations has identified potential early signs of disordered physiological functioning in populations undergoing intensely stressful events. Research on populations affected by Hurricane Andrew ties stress exposure to alterations in immune functioning, including reductions in natural killer cell cytotoxicity and numbers of CD-4 and CD-8 T cells (Ironson et al., 1997). There is, as yet, no clear evidence that these perturbations are linked to downstream health outcomes. This underscores, however, the importance of investigating the plasticity of the immune system and clarifying which immune system parameters should be included in future operationalizations of allostatic load. Post-traumatic stress disorder (PTSD) is associated in some studies with increased cortisol, epinephrine, norepinephrine, testosterone, and thyroxin functioning, changes that last over a long period of time (Wang and Mason, 1999). However, hypocortisolism has also been implicated in response to PTSD (Heim et al., 2000a; Thaller et al., 1999; Ehlert et al., 1999) and even for healthy individuals living under conditions of chronic stress (Heim et al., 2000b). Exposure to combat in war is tied to the development of deviant thyroid profiles. (Indeed, a history of traumatic stress is one of the

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