Exaggerated Stress Reponses in Adult Survivors of Childhood Abuse
Exaggerated Stress Reponses in Adult Survivors of Childhood Abuse
Abstract & Commentary
Source: Heim C, et al. Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. JAMA 2000;284:592-597.
Heim and colleagues assessed plasma adrenocorticotropic hormone (ACTH), cortisol levels, and heart rate in response to a standardized psychosocial laboratory stressor in adult women. Forty-nine female subjects 18-45 years of age were recruited to participate in the study. Subjects were divided into four groups: 1) women without a history of significant early-life stress and no psychiatric disorder (n = 12); 2) women with a history of childhood sexual and/or physical abuse with- out a Diagnostic and Statistical Manual of Mental Disor- ders, Fourth Edition (DSM-IV) diagnosis of current major depression (n = 14); 3) women with a history of childhood sexual and/or physical abuse and a DSM-IV diagnosis of current major depression (n = 13); and 4) women with a DSM-IV diagnosis of current major depression and no history of significant early-life stress (n = 10). Of those women who suffered childhood abuse, five of 14 not carrying a diagnosis of current depression met criteria for posttraumatic stress disorder (PTSD) while 11 of 13 meeting criteria for depression also met criteria for PTSD.
For the purposes of this study, "childhood sexual and/or physical abuse" is defined as repeated abuse, once a month for at least one year; sexual abuse, having been forced to touch another person’s intimate parts, having been touched in intimate parts, attempted or completed vaginal, oral, or anal intercourse; physical abuse, having been spanked, kicked, or choked in a way that left bruises or injuries, having been attacked with a weapon or tied up or locked in a room or a closet; or both sexual and physical abuse, occurring before the first menstrual period. The presence or absence of these early-life stressors was assessed using the Early Trauma Inventory (ETI), a structured interview assessing the number, frequency, duration, and subjective effect of physical, sexual, and emotional abuse and generally traumatic experiences. Heim et al also made efforts to validate the reports of abuse through court, social service, or medical records, or from family and friends, though not all subjects could provide such validation.
Subjects with significant medical illness, irregular menses, past or current presence of psychotic symptoms or bipolar disorder, or current presence of substance abuse or dependency, or eating disorders were excluded from the study. All subjects were free of psychotropic or hormonal medication with the exception of oral contraceptives.
Subjects in each of the four study groups underwent a standardized psychosocial stress test performed between 1:30 and 4:30 PM. The stress protocol consisted of a 10-minute anticipation and preparation phase followed by a 10-minute public speaking and mental arithmetic task performed in front of an audience. Blood samples from indwelling catheters and heart-rate levels were obtained in 15-minute intervals before (15 minutes and 0 minutes), during (15 minutes), and after (30, 45, 60, 75, 90 minutes) the stress exposure. Plasma was assayed for ACTH and cortisol concentrations by blinded members of the research team.
The stress test induced significant increases in mean ACTH, cortisol, and heart rate levels across all groups. Mean ACTH levels of the four groups differed significantly at 15 minutes and 30 minutes after the start of stress induction. Abused women with and without cur- rent major depression exhibited increased ACTH con- centrations compared to controls and depressed women who were not abused. Additionally, maximum ACTH levels minus baseline values were more than six-fold higher in abused women with depression (net peak, 9.0 pmol/L) than in controls (net peak, 1.4 pmol/L). Abused women with current depression also exhibited higher cortisol responses than all other groups at 30 and 60 minutes after stress induction, as well as increased maximum levels of cortisol when compared to all other groups. Significant differences in heart rate were found between groups at 15 minutes after induction of stress with abused women with current major depression demonstrating higher heart rate responses compared to controls. This group also showed higher mean maximum heart rates than controls, (89.7 vs 78.4 beats/minute).
COMMENT BY Lauren B. Marangell, MD & Christopher D. Martin
Heim et al have presented an elegant study demonstrating persistent sensitization of the pituitary-adrenal and autonomic stress response in adult women survivors of childhood sexual and/or physical abuse. As Heim et al point out, this is the first human study to report persistent changes in stress reactivity in adult survivors of early-life trauma. The interplay of biological and environmental factors in the etiology of psychiatric disorders has long been the subject of much discussion. Early adverse experiences are known to have an association with development of mood and anxiety disorders later in life. It is likely that the persistent sensitization of the pitu- itary-adrenal axis and autonomic hyperactivity demon- strated by Heim et al in these victims of severe early-life trauma may contribute to a diathesis predisposing cer- tain individuals to development of disorders such as major depressive disorder and PTSD in adult life. Heim et al implicate hypersecretion of corticotropin-releasing factor (CRF) as the etiologic mechanism of this sensi- tized state, important because in addition to potentially producing the physiologic results seen in this study, CRF has been shown to produce symptoms consistent with depression and anxiety when administered directly into the CNS of animals in laboratory studies.
The results of this study shed new light upon the issue of patients with a previous history of childhood abuse. Heim et al present evidence suggesting that early-life trauma may precipitate a persistent biological state which may function as a true risk factor for the development of psychiatric disease later in life. Thus, in a clinical setting, a history of childhood abuse must be viewed as a relevant factor with current bearing upon a patient’s risk of developing disease, much as an extensive history of cigarette smoking places a patient at increased risk of developing bronchogenic carcinoma. In both cases, the physician must be vigilant in observing the patient for signs of developing disease.
Also of note, the results demonstrate that while depressed subjects with a history of childhood abuse showed persistent sensitization to stress, depressed subjects with no history of severe early-life stress demonstrated normal stress reactivity. This finding suggests that the depression experienced by each of these two groups may arise from different etiologies. Thus, these groups may suffer from different subtypes of depression with differing pathophysiology. This is an interesting area for future investigation.
Heim et al comment on recent studies in murine models, which show the ability of antidepressant treatment with paroxetine and reboxetine to reverse CRF hypersecretion and other neurobiological consequences of maternal separation. These data show promise regarding potential treatments for adult survivors of childhood trauma with depression/anxiety and persistent sensitization to stress. Antidepressants may also have a role as preventative therapy in patients who have been exposed to early-life trauma, developing hyperactive hormonal and autonomic stress responses and a predisposition to adult mood and anxiety disorders, though not yet suffer-ing from diagnosable psychiatric disorders. Heim et al also touch upon the prospect of using CRF receptor antagonists as treatment for mood and/or anxiety disorders in this population. Currently, research is underway to assess the efficacy of this approach. The pertinent question remains, will psychopharmacologic or psychotherapeutic treatments reverse the biological vulnerability to develop disorders described by Heim et al? (Christopher Martin is an associate in the Mood Disorders Center, Baylor College of Medicine, Houston, Tex.)
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