Effect of childhood physical abuse on cortisol stress response
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Abuse and neglect are highly prevalent in children and have enduring neurobiological effects. Stressful early life environments perturb the hypothalamic–pituitary–adrenal (HPA) axis, which in turn may predispose to psychiatric disorders in adulthood. However, studies of childhood maltreatment and adult HPA function have not yet rigorously investigated the differential effects of maltreatment subtypes, including physical abuse.
In this study, we sought to replicate our previous finding that childhood maltreatment was associated with attenuated cortisol responses to stress and determine whether the type of maltreatment was a determinant of the stress response.
Salivary cortisol response to the Trier Social Stress Test (TSST) was examined in a non-clinical sample of women (n = 110). Subjects had no acute medical problems and were not seeking psychiatric treatment. Effects of five maltreatment types, as measured by the Childhood Trauma Questionnaire, on cortisol response to the TSST were investigated. To further examine the significant (p < 0.005) effect of one maltreatment type, women with childhood physical abuse (PA) (n = 20) were compared to those without past PA (n = 90).
Women reporting childhood PA displayed a significantly blunted cortisol response to the TSST compared with subjects without PA, after controlling for estrogen use, age, other forms of maltreatment, and other potential confounds. There were no differences between PA and control groups with regard to physiological arousal during the stress challenge.
In a non-clinical sample of women with minimal or no current psychopathology, physical abuse is associated with a blunted cortisol response to a psychosocial stress task.
KeywordsChildhood Trauma Stress Physical abuse Cortisol HPA axis Saliva
Funding for this study was provided by NIMH Grant R01 MH068767 (LLC) and K23 MH067947 (ART). The authors report no disclosures relevant to this work. No therapeutic pharmaceutical or device products were utilized in this research protocol. The authors disclose the following biomedical financial interests and sources of support over the past 3 years and the foreseeable future. Drs. Tyrka, Price, and Carpenter have received grant/research support from the National Institutes of Health, NARSAD, Department of Defense, Sepracor, Cyberonics, Neuronetics, UCB Pharma, and Medtronic. Dr. Tyrka received honoraria for continuing medical education from Lundbeck and Takeda. Dr. Price has received speakers’ bureau honoraria from Jazz Pharmaceuticals and MD Conferences/Psychiatry Review Course, consultant income from Abbott, Gerson Lehrman, Wiley, Qatar National Research Fund, Alberta Heritage Foundation for Medical Research, Springer, and Lundbeck. Dr. Carpenter has served as a consultant or on an advisory board for Abbott, AstraZeneca, Cyberonics, Novartis, Neuronetics, and Wyeth, and has received honoraria for continuing medical education from AstraZeneca and speakers’ bureau honoraria from Cyberonics and Neuronetics. Dr. Geracioti received grant support from the National Institutes of Health, the Department of Veterans Affairs, and the Department of Defense; he is the principal equity holder of RxDino, LLC, a pharmaceutical company which is developing dual corticosteroids for dermatological indications. Dr. Thaddeus Shattuck discloses no outside support. The authors thank Kelly Colombo, B.A. for her assistance with data management and Nosa N. Ekhator, M.S. for his technical facility with the salivary cortisol assays.
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