The neural regulation of responses to threat ultimately affects downstream biological stress regulatory systems. What are these systems? During times of stress, the body releases the catecholamines epinephrine and norepinephrine with concomitant sympathetic nervous system arousal. Stress may also engage the HPA (hypothalamic-pituitary-adrenocortical) axis, involving the release of corticosteroids including cortisol. These responses have short-term protective effects under stressful circumstances, because they mobilize the body to meet the demands of pressing situations. However, with chronic or recurrent activation, they can be associated with deleterious long-term implications for health (e.g., Seeman and McEwen, 1996; Uchino et al, 1996, see Chapter 42). For example, excessive or repeated discharge of epinephrine or norepinephrine can lead to the suppression of cellular immune function, produce hemodynamic changes such as increases in blood pressure and heart rate, provoke abnormal heart rhythms such as ventricular arrhythmias, and produce neurochemical imbalances that may relate to psychiatric disorders. Intense, rapid, and/or long-lasting sympathetic responses to repeated stress or challenge have been implicated in the development of hypertension and coronary artery disease (McEwen and Stellar, 1993).
Stress can also suppress immune functioning in ways that leave a person vulnerable to opportunistic diseases and infections. Corticosteroids such as cortisol have immunosuppressive effects, and stress-related increases in cortisol have been tied to decreased lymphocyte responsivity to mitogenic stimulation and to decreased lymphocyte cytotoxicity. Such immunosuppressive changes may be associated with increased susceptibility to infectious disorders and to destruction of neurons in the hippocampus as well (McEwen and Sapolsky, 1995). Chronic stress can also diminish the immune system's sensitivity to glucocorticoid hormones that normally terminate the inflammatory cascade that occurs during stress (Miller et al, 2002).
Extensive evidence suggests that these systems - the HPA axis, the immune system, and the sympathetic nervous system - influence each other and thereby affect each other's functioning. To the extent, then, that early environment influences the affective states and socioemotional skills that can keep sympathetic nervous system and HPA axis responses to stress low, it may have a beneficial impact on other systems as well (Seeman and McEwen, 1996; Uchino et al, 1996). In turn, these may beneficially affect health.
Correspondingly, a lack of supportive contacts in early childhood has been tied to higher autonomic responses to stress in children (e.g.,
El-Sheikh et al, 1989) and to higher HPA axis responses to stressors in children (Gunnar et al, 1992). Studies of young adults reveal that a harsh early family environment is tied to elevated auto-nomic responses to a laboratory stressor and to an elevated flat cortisol response to laboratory stressors (Taylor et al, 2004). Thus, the existing literature provides a strong basis for pathways linking a stressful early childhood to high reactivity of biological stress regulatory systems.
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