Yehuda R. Current status of cortisol findings in post-traumatic stress disorder. Psychiatr Clin North Am 25: 341-368
ABSTRACT This article summarizes findings of hypothalamic-pituitary-adrenal axis alterations in post-traumatic stress disorder (PTSD) and evaluates likely reasons for the lack of agreement among published studies. Sources of variance caused by methodologic and interpretative differences are highlighted, but the disparate findings are explained as illustrating a more complex neuroendocrinology of PTSD than has previously been described.
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- ", 2014 ; Suzuki et al . , 2013 ; Yehuda , 2002 ) . With respect to HCC specifically , while some studies of PTSD have found elevated HCC in such patients ( Steudte , Stalder et al . "
ABSTRACT: Hair cortisol concentrations (HCC) are receiving increased attention as a novel biomarker of psychophysiological responses to chronic stress, with potential relevance for psychopathology risk research. We examined the validity of HCC as a marker of psychosocial stress in mother (Mage = 37.87 years)-daughter (Mage = 7.62 years) dyads characterized by higher (n = 30) or lower (n = 30) maternal chronic stress. Additionally, we examined whether early care moderated similarity of HCC levels within dyads. Higher-stress mothers had significantly lower HCC compared to lower-stress mothers, consistent with other research showing that chronic stress leads to blunted HPA axis activity over time. Further, HCC in daughters were significantly and positively associated with previously assessed salivary cortisol stress reactivity. Finally, mother-daughter HCC associations were significantly moderated by negative parenting styles, such that associations became stronger as quality of parenting decreased. Findings overall indicate that HCC may be a useful marker of cortisol responses to chronic stress. © 2015 Wiley Periodicals, Inc. Dev Psychobiol. © 2015 Wiley Periodicals, Inc.Developmental Psychobiology 04/2015; 57(5). DOI:10.1002/dev.21302 · 3.31 Impact Factor
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- "Danielson et al . Theories that speak to this link between altered HPA axis functioning and PTSD suggest that low levels of cortisol , or hypocortisolism , may negatively impact the metabolic , immuno - and neurodefensive processes necessary for cop - ing adaptively with acute stressors ( Yehuda , 2002 ) . That is , instead of the potentially adaptive pattern of HPA - axis acti - vation ( i . "
ABSTRACT: Parental Posttraumatic Stress Disorder (PTSD), particularly maternal PTSD, confers risk for stress-related psychopathology among offspring. Altered hypothalamic-pituitary-adrenal (HPA) axis functioning is one mechanism proposed to explain transmission of this intergenerational risk. Investigation of this mechanism has been largely limited to general stress response (e.g., diurnal cortisol), rather than reactivity in response to an acute stressor. We examined cortisol reactivity in response to a laboratory stressor among offspring of mothers with a lifetime diagnosis of PTSD (n=36) and age- and gender- matched control offspring of mothers without PTSD (n=36). Youth (67% girls; mean age=11.4, SD=2.6) participated in a developmentally sensitive laboratory stressor and had salivary cortisol assessed five times (one pre-stress, one immediate post-stress, and three recovery measures, spaced 15min apart). Results were consistent with the hypothesis that offspring of mothers with PTSD would exhibit a dysregulated, blunted cortisol reactivity profile, and control offspring would display the expected adaptive peak in cortisol response to challenge profile. Findings were maintained after controlling for youth traumatic event history, physical anxiety symptoms, and depression, as well as maternal depression. This finding contributes to the existing literature indicating that attenuated HPA axis functioning, inclusive of hyposecretion of cortisol in response to acute stress, is robust among youth of mothers with PTSD. Future research is warranted in elucidating cortisol reactivity as a link between maternal PTSD and stress-related psychopathology vulnerability among offspring. Copyright © 2015 Elsevier Ltd. All rights reserved.Psychoneuroendocrinology 01/2015; 53C:170-178. DOI:10.1016/j.psyneuen.2015.01.001 · 4.94 Impact Factor
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- "They fail to trigger the negative feedback loop, thus prolonging the adrenergic response, which may exacerbate consolidation of the traumatic memory. This may lead to intrusive symptoms, which may increase the risk for PTSD (Yehuda, 2002). "
ABSTRACT: Background Decreased activation of the hypothalamus-pituitary-adrenal (HPA) axis in response to stress is suspected to be a vulnerability factor for posttraumatic stress disorder (PTSD). Previous studies showed inconsistent findings regarding the role of cortisol in predicting PTSD. In addition, no prospective studies have examined the role of dehydroepiandrosterone (DHEA), or its sulfate form DHEAS, and the cortisol-to-DHEA(S) ratio in predicting PTSD. In this study, we tested whether acute plasma cortisol, DHEAS and the cortisol-to-DHEAS ratio predicted PTSD symptoms at 6 weeks and 6 months post-trauma. Methods Blood samples of 397 adult level-1 trauma center patients, taken at the trauma resuscitation room within hours after the injury, were analyzed for cortisol and DHEAS levels. PTSD symptoms were assessed at 6 weeks and 6 months post-trauma with the Clinician Administered PTSD Scale. Results Multivariate linear regression analyses showed that lower cortisol predicted PTSD symptoms at both 6 weeks and 6 months, controlling for age, gender, time of blood sampling, injury, trauma history, and admission to intensive care. Higher DHEAS and a smaller cortisol-to-DHEAS ratio predicted PTSD symptoms at 6 weeks, but not after controlling for the same variables, and not at 6 months. Conclusions Our study provides important new evidence on the crucial role of the HPA-axis in response to trauma by showing that acute cortisol and DHEAS levels predict PTSD symptoms in survivors of recent trauma.Psychoneuroendocrinology 07/2014; 45. DOI:10.1016/j.psyneuen.2014.04.001 · 4.94 Impact Factor