Deficits in socioemotional skills may ultimately stabilize into enduring risks for emotional disorders, such as anxiety, depression, and other chronic negative emotional states. These states may act as predisposing factors for adverse physical health outcomes (Hemingway et al, 2003). For example, hostility has been tied to the development of metabolic syndrome among children and adolescents (Dembroski et al, 1985) and to an increased risk for coronary heart disease (CHD) and hypertension (Julkunen et al, 1994). Major depression, depressive symptoms, and history of depression have all been identified as predictors of cardiac events (Frasure-Smith et al, 1995), and depression is a risk factor for mortality following myocardial infarction, independent of cardiac disease severity (Frasure-Smith et al, 1995). State depression, as well as clinical depression, have been related to sustained suppressed immunity (Herbert and Cohen, 1993). Anger appears to play a significant role in the development of coronary artery disease and hypertension, at least among some individuals (e.g., Julkunen et al, 1994; Smith,
1992). Depression and anxiety are implicated in numerous health risks, including all-cause mortality (Martin et al, 1995), and evidence points to a dose-response relation between anxiety and coronary heart disease (Kubzansky et al, 1998).
Links between negative emotional states and health outcomes may result from chronic or recurring engagement of biological stress regulatory systems. Negative emotional states have been tied to heightened biological stress responses, including evidence of stronger autonomic response to stressful circumstances (e.g., Matthews et al, 1996) and stronger hypothalamic-pituitary-adrenocortical (HPA) responses to stress (e.g., Chorpita and Barlow, 1998; Flinn and England, 1997). Studies also suggest links between negative emotions and reduced heart rate variability (e.g., Kawachi et al, 1995), implicating potential compromises in parasympathetic functioning in these relations. Intense, chronic, or recurring biological responses to stress may, thus, represent one pathway by which a harsh early environment exerts adverse effects on adult health outcomes (McEwen, 1998; Repetti et al, 2002), effects that may be mediated, at least in part, by negative emotional states.
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