Journal
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
Volume 256, Issue 3, Pages 174-186Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00406-005-0624-4
Keywords
child development; neurobiology; stress; childhood abuse; domestic violence; substance; mental health
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Funding
- NCRR NIH HHS [S10 RR016917-01, S10 RR016917] Funding Source: Medline
- NHLBI NIH HHS [R01 HL088726, R01 HL088726-04] Funding Source: Medline
- NIMH NIH HHS [K24 MH076955, R01 MH056120-12, R01 MH056120, T32 MH067547, T32 MH067547-05, R21 MH080208-02, K24 MH076955-05, R21 MH080208] Funding Source: Medline
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Background Childhood maltreatment has been linked to a variety of changes in brain structure and function and stress-responsive neurobiological systems. Epidemiological studies have documented the impact of childhood maltreatment on health and emotional well-being. Methods After a brief review of the neurobiology of childhood trauma, we use the Adverse Childhood Experiences (ACE) Study as an epidemiological case example of the convergence between epidemiologic and neurobiological evidence of the effects of childhood trauma. The ACE Study included 17,337 adult HMO members and assessed 8 adverse childhood experiences (ACEs) including abuse, witnessing domestic violence, and serious household dysfunction. We used the number of ACEs (ACE score) as a measure of cumulative childhood stress and hypothesized a dose-response relationship of the ACE score to 18 selected outcomes and to the total number of these outcomes (comorbidity). Results Based upon logistic regression analysis, the risk of every outcome in the affective, somatic, substance abuse, memory, sexual, and aggression-related domains increased in a graded fashion as the ACE score increased (P < 0.001). The mean number of comorbid outcomes tripled across the range of the ACE score. Conclusions The graded relationship of the ACE score to 18 different outcomes in multiple domains theoretically parallels the cumulative exposure of the developing brain to the stress response with resulting impairment in multiple brain structures and functions.
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