The authors examined the relationships among history of previous assault, severity of rape, acute plasma cortisol level after rape, and development of rape-related post-traumatic stress disorder (PTSD).
Blood samples were drawn from 37 adult female rape victims within 51 hours after they had been raped. The subjects were assessed for history of previous assault and for the presence of PTSD 17-157 days (mean = 90 days) after the rape.
Women with a history of previous assault had a lower mean acute cortisol level after the rape but a higher probability of subsequently developing PTSD. A significant interaction between history of previous assault and the severity of the index rape was observed: only women who had never been assaulted before had higher cortisol levels following high-severity rapes (those which included injury or multiple types of penetration) than low-severity rapes.
The authors conclude that previous traumatization may attenuate the acute cortisol response to trauma.
"with alterations in physiological reactivity to subsequent mental stress in women " and that even one incident of traumatic abuse, even in (previously) " healthy " women (apparently free of psychological complaints), could have such a result (Girdler et al. 2003, 849). Resnick et al. (1995) showed similar findings and Girdler et al. (2007) found that all women who had suffered abuse showed changes in their biological stress-responsive systems, whether they were diagnosed with PMDD or among the non-PMDD controls. Another study found that a history of sexual abuse was associated with elevated thyroid-stimulating hormone concentrations, regardless of PMS or PMDD (Bunevicius, Leserman, and Girdler 2012). "
[Show abstract][Hide abstract] ABSTRACT: Premenstrual dysphoric disorder (PMDD) was recently moved to a full category in the DSM-5 (the latest edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders). It also appears set for inclusion as a separate disorder in the ICD-11 (the upcoming edition of the World Health Organization's International Statistical Classification of Diseases and Related Health Problems). This paper argues that PMDD should not be listed in the DSM or the ICD at all, adding to the call to recognise PMDD as a socially constructed disorder. I first present the argument that PMDD pathologises understandable anger/distress and that to do so is potentially dangerous. I then present evidence that PMDD is a culture-bound phenomenon, not a universal one. I also argue that even if (1) medication produces a desired effect, (2) there are biological correlates with premenstrual anger/distress, (3) such anger/distress seems to occur monthly, and (4) women are more likely than men to be diagnosed with affective disorders, none of these factors substantiates that premenstrual anger/distress is caused by a mental disorder. I argue that to assume they do is to ignore the now accepted role that one's environment and psychology play in illness development, as well as arguments concerning the social construction of mental illness. In doing so, I do not claim that there are no women who experience premenstrual distress or that their distress is not a lived experience. My point is that such distress can be recognised and considered significant without being pathologised and that it is unethical to describe premenstrual anger/distress as a mental disorder. Further, if the credibility of women's suffering is subject to doubt without a clinical diagnosis, then the way to address this problem is to change societal attitudes towards women's suffering, not to label women as mentally ill. The paper concludes with some broader implications for women and society of the change in status of PMDD in the DSM-5 as well as a sketch of critical policy suggestions to address these implications.
"There is a growing body of literature that supports the match/mismatch hypothesis: in rodents, the effects of early life stress are less pronounced under negative juvenile and adult environment (Buwalda et al., 2013; Daskalakis et al., 2012; Raftogianni et al., 2012; Ricon et al., 2012). Also in humans there are indications that life time adversity can buffer the response to an acute adult life stress (Elzinga et al., 2008; Resnick et al., 1995). Indeed, even though mostly unintentional, most of the early studies on early life or adult stress only used one stress procedure (either early in life or in adulthood ), thereby always creating developmentally mismatched environmental conditions. "
[Show abstract][Hide abstract] ABSTRACT: Chronic stress is one of the predominant environmental risk factors for a number of psychiatric disorders, particularly for major depression. Different hypotheses have been formulated to address the interaction between early and adult chronic stress in psychiatric disease vulnerability. The match/mismatch hypothesis of psychiatric disease states that the early life environment shapes coping strategies in a manner that enables individuals to optimally face similar environments later in life. We tested this hypothesis in female Balb/c mice that underwent either stress or enrichment early in life and were in adulthood further subdivided in single or group housed, in order to provide aversive or positive adult environments, respectively. We studied the effects of the environmental manipulation on anxiety-like, depressive-like and sociability behaviours and gene expression profiles. We show that continuous exposure to adverse environments (matched condition) is not necessarily resulting in an opposite phenotype compared to a continuous supportive environment (matched condition). Rather, animals with mismatched environmental conditions behaved differently from animals with matched environments on anxious, social and depressive like phenotypes. These results further support the match/mismatch hypothesis and illustrate how mild or moderate aversive conditions during development can shape an individual to be optimally adapted to similar conditions later in life.
European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 06/2014; 24(6). DOI:10.1016/j.euroneuro.2014.02.002 · 4.37 Impact Factor
"Hence, the method offered a feasible means for classifying animal response patterns to trauma, thereby increasing the conceptual accuracy of the data and offered an additional study parameter, namely " prevalence " (Cohen et al. 2003, 2005; Cohen and Zohar 2004). Notably, the proportion of the entire exposed population fulfilling criteria for extreme responses (EBR) was compatible with epidemiological data for PTSD amongst trauma-exposed human populations (Breslau et al. 1991); these data report that between 15–35 % fulfill criteria for PTSD and that approximately 20–30 % display partial or sub-symptomatic clinical pictures (Breslau et al. 1998; Resnick et al. 1995). "
[Show abstract][Hide abstract] ABSTRACT: Post-traumatic stress disorder (PTSD) is clinically defined in DSM-4 by exposure to a significantly threatening and/or horrifying event and the presence of a certain number of symptoms from each of three symptom clusters at least one month after the event. Since humans clearly do not respond homogeneously to a potentially traumatic experience, the heterogeneity in animal responses might be regarded as confirming the validity of animal studies, rather than as representing a problem. A model of diagnostic criteria for psychiatric disorders could therefore be applied to animal responses to augment the validity of study data, providing that the criteria for classification are clearly defined, reliably reproducible and yield results that conform to findings in human subjects. The method described herein was developed in an attempt to model diagnostic criteria in terms of individual patterns of response by using behavioral measures and determining cut-off scores to distinguish between extremes of response or non-response, leaving a sizeable proportion of subjects in a middle group, outside each set of cut-off criteria. The cumulative results of our studies indicate that the contribution of animal models can be further enhanced by classifying individual animal study subjects according to their response patterns. The animal model also enables the researcher to go one step further and correlate specific anatomic, bio-molecular and physiological parameters with the degree and pattern of the individual behavioral response and introduces "prevalence rates" as a parameter. The translational value of the classification method and future directions are discussed.
Cell and Tissue Research 08/2013; 354(1). DOI:10.1007/s00441-013-1687-6 · 3.57 Impact Factor
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