Original articleEarly physical and sexual abuse associated with an adverse course of bipolar illness
Introduction
Aconsiderable literature implicates psychosocial stresses in the onset and initial recurrence of the unipolar and bipolar affective disorders Kraepelin 1921, Brown and Harris 1978, Post et al 2000, but with increasing numbers of subsequent recurrences, episodes are more likely to occur more rapidly and autonomously Ghaemi et al 1999, Kessing et al 1998, Post et al 1996, Post et al 2000. Most of these studies, however, examine the occurrence of psychosocial stressors in adulthood Brown and Harris 1978, Paykel et al 1969. Although many studies have looked at possible links between early traumatic events and development of psychopathology over the life span Breslau et al 1998, Brown and Anderson 1991, Bryer et al 1987, Grilo et al 1999, Kaplan et al 1998, Kessler et al 1997, Levitan et al 1998, McCauley et al 1997, Moncrieff et al 1996, Moncrieff and Farmer 1998, Mullen et al 1995, Ogata et al 1990, Pope and Hudson 1992, Rorty et al 1994, Ruggiero et al 1999, Schaaf and McCanne 1998, Stein et al 1996, Wexler et al 1997, Young et al 1997, few studies Bauer et al 1997, Levitan et al 1998 have examined the potential role of early life stresses (and those of particularly high severity involving physical or sexual abuse in childhood and adolescence) on the subsequent course of bipolar illness.
Nonetheless, early stressful life experiences have been postulated to act as vulnerability factors and provide an underlying neural substrate for the subsequent provocation of affective disorders by stressors occurring in adulthood (Post 1992). A substantial preclinical literature supports this view, with perinatal experience of single, prolonged, 24-hour (Levine et al 1991; Zhang et al unpublished) or repeated 3-hour maternal separations of the neonatal rat pup Caldji et al 2000, Francis et al 1999, Meaney et al 1993, resulting in long-lasting alterations in anxiety-related behavior, hypercortisolemia, and proneness to cocaine and alcohol self-administration.
Given this literature on the potential long-lasting consequences of early adverse environmental experiences on affective behavior, neurochemistry, and brain structure Gould et al 1998, Kaufman et al 2000, Meaney et al 1993, Plotsky et al 1998, we wished to specifically explore the potential association of physical or sexual abuse in childhood or adolescence with illness characteristics and the course of bipolar disorder. Our hypothesis was that the occurrence of these traumatic events early in life would add to the vulnerability for development and recurrence of affective episodes, presaging a more severe course of bipolar illness.
Section snippets
Methods and materials
Patients included in this study were participating in the five sites of the Stanley Foundation Bipolar Treatment Outcome Network (SFBN) Leverich et al in press, Suppes et al in press, were 18 years or older, and had a DSM-IV (American Psychiatric Association, 1994) diagnosis of bipolar I (BPI), bipolar II (BPII), or bipolar NOS (BPNOS) as determined by the SCID-P (First et al 1996), a detailed clinician-administered questionnaire, or both. The correlation between the SCID-P and clinician
Results
In this analysis, we included 631 consecutive patients with complete admission data sets who were enrolled in the SFBN. Of 377 female patients, 185 (49%) reported having experienced early abuse in childhood or adolescence; physical abuse was reported in 36.0% and sexual abuse in 43.4% of the women. Of 274 male patients, 99 (36%) reported ever having been abused in childhood or adolescence; 30.8% of these men reported physical and 21.2% reported sexual abuse. Of the patient group who reported
Discussion
Although a number of studies have explored the long-term neurobiological effects of childhood and adolescent physical and sexual abuse De Bellis et al 1999a, De Bellis et al 1999b, Putnam and Trickett 1993, Putnam and Trickett 1997, Stein et al 1997, as well as behavioral changes and subsequent development of psychiatric illnesses Briere and Runtz 1990, Brown and Anderson 1991, Brown et al 1998, Kaplan et al 1999, Markowitz 1994, Simpson et al 1994, Stein et al 1996, Wexler et al 1997, Young et
Acknowledgements
The authors would like to acknowledge the generous support from the Theodore and Vada Stanley Foundation. The authors acknowledge the excellent additional analytic work of Sara Perez and David Luckenbaugh.
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