مقاله انگلیسی رایگان در مورد پاسخ های آلفا آمیلاز به استرس روانی- اجتماعی – الزویر 2018

Hypothalamic-pituitary-adrenal axis (HPA) and sympathetic-adrenomedullary system (SAM) co-activation has been implicated in the development of psychopathology (Bauer, Quas, & Boyce, 2002; Hastings et al., 2011), leading to the need to understand individual differences in HPA–SAM co-activation in childhood and adolescence. Theorists have posited that both symmetrical (e.g., high HPA–high SAM, low HPA–low SAM) and asymmetrical (e.g., low HPA–high SAM, high HPA–low SAM) activity is potentially reflective of neuroendocrine response dysregulation linked to children’s internalizing and externalizing behavior (Bauer et al., 2002). When assessed via HPA (salivary costisol, sC) and SAM (salivary alpha-amylase, sAA) indices in response to laboratory stressor paradigms, early adolescent studies have found mixed support for each proposition. Thus, there remains a lack of consensus on what constitutes well-functioning as well as dysregulated HPA-SAM co-activation response patterns. The evidence supporting these views is based on variable-centered approaches that assume preadolescents exhibit more or less the same pattern of HPA–SAM co-activation. However, theory suggests that preadolescence is a period of substantive reformation to the HPA and SAM, when children are exposed to novel psychosocial stressors that shape their development (Spear, 2000; Steinberg, 2014). If so, then variable-centered approaches may overlook the possibility that certain subgroups of children evidence qualitatively distinct patterns of HPA–SAM co-activation that may be uniquely linked to their behavioral adjustment. Person-centered approaches that incorporate multiple, theory-driven neuroendocrine response indices (e.g., sC, sAA) have the potential to identify these subgroups. Such an approach may also provide a more precise approximation of theoretical cross-system activation patterns (Bauer et al., 2002) that index healthy functioning or signal risk for psychopathological development (Rutter, 2007). Children’s coping, defined as effortful emotional, cognitive, and behavioral attempts to manage a stressor or children’s emotional/cognitive/behavioral reactions to it, is thought to buffer against such psychopathological development by mitigating against one of the mechanisms of risk; neuroendocrine response dysregulation (Wadsworth, 2015). Recent evidence suggests that children’s coping does in fact get “underneath the skin” (Foland-Ross, Kircanski, & Gotlib, 2014; Sladek, Doane, & Stroud, 2017), supporting quick, efficient recovery of stressorinduced neuroendocrine activation (Stewart, Mazurka, Bond, WynneEdwards, & Harkness, 2013). This research points to putative mechanisms of change to be leveraged in the design of coping interventions (Davidson & McEwen, 2012). However, reliance on variablecentered designs has limited understanding about for whom certain types of coping combat the potentially damaging effects of stress.