Transgenerational transmission of cortisol and PTSD risk. Prog
The Traumatic Stress Studies Program, Department of Psychiatry, Mount Sinai School of Medicine and Bronx Veterans Affairs, James J Peters VAMC, 116-A, OOMH-PTSD, Bronx, NY 10468, USA.Progress in brain research (Impact Factor: 2.83). 02/2008; 167:121-35. DOI: 10.1016/S0079-6123(07)67009-5
Parental posttraumatic stress disorder (PTSD) appears to be a relevant risk factor for the development of PTSD, as evidenced by a greater prevalence of PTSD, but not trauma exposure, in adult offspring of Holocaust survivors with PTSD, compared to children of Holocaust-exposed parents without PTSD. This paper summarizes recent neuroendocrine studies in offspring of parents with PTSD. Offspring of trauma survivors with PTSD show significantly lower 24-h mean urinary cortisol excretion and salivary cortisol levels as well as enhanced plasma cortisol suppression in response to low dose dexamethasone administration than offspring of survivors without PTSD. In all cases, neuroendocrine measures were negatively correlated with severity of parental PTSD symptoms, even after controlling for PTSD and even other symptoms in offspring. Though the majority of our work has focused on adult offspring of Holocaust survivors, recent observations in infants born to mothers who were pregnant on 9/11 demonstrate that low cortisol in relation to parental PTSD appears to be present early in the course of development and may be influenced by in utero factors such as glucocorticoid programming. Since low cortisol levels are particularly associated with the presence of maternal PTSD the findings suggest the involvement of epigenetic mechanisms.
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- "du stress chez ce dernier (Gowin et al., 2013 ;Neigh, Gillespie, & Nemeroff, 2009 ;Yehuda & Bierer, 2008). Au plan transgénérationnel, des altérations du HPA et des taux de cortisol plus bas ont été retrouvés chez les enfants de mères ayant vécu des sévices dans l'enfance – en particulier lorsque jumelés à d'autres psychopathologies (ÉSPT, dépression) ou facteurs de stress chez la mère (Brand et al., 2010) – suggérant que certains phénomènes épigénétiques corrélés aux situations de maltraitance à la première génération pourraient se transmettre à la suivante (Neigh et al., 2009). "
ABSTRACT: Literature review on clinical issues with parents at risk of child abuse: targeting the generational factor? The prevalence of child abuse is higher in families with psychosocial vulnerabilities or when one or both parents experienced abuse or neglect during childhood. While the most widespread intervention approaches in Canada (e.g. material support or parenting skills programs) show mixed results in providing changes in mistreatment cycles, we examine clinical practice focused on generational repetition of trauma. In order to explore this topic, this paper has 4 objectives and will be supported by a narrative review of the literature: 1) to document the causalities of child maltreatment; 2) to identify the clinical challenges of struggling parents; 3) to develop a critical analysis of the intervention programs commonly spread in Canada; 4) to take into account multifaceted vulnerabilities of these families through innovative practice perspectives.
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- "Sigal and Rakoff (1971) reported that survivors' children shared severe depressive symptomatology, school problems , and excessive quarreling with siblings. Particularly in the context of parental psychopathology, offspring experience increased anxiety and depression (Gangi, Talamo, & Ferracuti, 2009), posttraumatic stress disorder (Leen-Feldner et al., 2013; Sigal, 1999; Yehuda & Bierer, 2007), and low self-esteem (Gangi et al., 2009). When compared with controls, children of survivors tend to experience mistrust, have difficulties expressing emotions and regulating aggression (Eaton, Sigal, & Weinfeld, 1982; Felsen, 1998), and may have an impaired potential for posttraumatic growth following their own traumas (Dekel, Mandl, & Solomon, 2013). "
ABSTRACT: The impacts of the Holocaust on children of survivors have been widely investigated. However, consensus is limited, and no validated measures have been tailored with or to them. We aimed to develop and validate a scale that measures these specific impacts (Part II of the Danieli Inventory of Multigenerational Legacies of Trauma). We studied 484 adult children of survivors who participated in a cross-sectional web-based survey in English or Hebrew; of these, 191 participated in a clinical interview. Exploratory factor analyses of 58 items to reduce and refine the measure yielded a 36-item scale, Reparative Adaptational Impacts, that had excellent internal consistency (α = .91) and congruence between English and Hebrew versions (φ ≥ .95). Associations between impacts and SCID-based diagnoses of major depressive episode, posttraumatic stress disorder, and generalized anxiety disorder were moderate to strong (ds = 0.48-0.89). Strong associations also emerged between severity of offspring's reparative adaptational impacts and intensity of their parents' posttrauma adaptational styles (Multiple R = .72), with intensity of victim style, especially the mother's, having the strongest effect (β = .31-.33). Having both research and clinical relevance for assessing Holocaust survivors' offspring, future studies might investigate the scale's generalizability to other populations affected by mass trauma. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
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- "Telomere length in complex PTSD has not been specifically investigated so far. Interestingly, epigenetic alterations or changes in telomere length may also show transgenerational effects (Kü ffer, Maercker, & Burri, 2014; Yehuda & Bierer, 2008). Some major biological findings relevant to PTSD and pilot data concerning complex PTSD are summarized in Table 3. "
ABSTRACT: Complex posttraumatic stress disorder (PTSD) presents with clinical features of full or partial PTSD (re-experiencing a traumatic event, avoiding reminders of the event, and a state of hyperarousal) together with symptoms from three additional clusters (problems in emotional regulation, negative self-concept, and problems in interpersonal relations). Complex PTSD is proposed as a new diagnostic entity in ICD-11 and typically occurs after prolonged and complex trauma. Here we shortly review current knowledge regarding the biological correlates of complex PTSD and compare it to the relevant findings in PTSD. Recent studies provide support to the validity of complex PTSD as a separate diagnostic entity; however, data regarding the biological basis of the disorder are still very limited at this time. Further studies focused on complex PTSD biological correlates and replication of the initial findings are needed, including neuroimaging, neurobiochemical, genetic, and epigenetic investigations. Identification of altered biological pathways in complex PTSD may be critical to further understand the pathophysiology and optimize treatment strategies.
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