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      The enduring effects of abuse and related adverse experiences in childhood : A convergence of evidence from neurobiology and epidemiology

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          Abstract

          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. 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). 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. 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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          More hippocampal neurons in adult mice living in an enriched environment.

          Neurogenesis occurs in the dentate gyrus of the hippocampus throughout the life of a rodent, but the function of these new neurons and the mechanisms that regulate their birth are unknown. Here we show that significantly more new neurons exist in the dentate gyrus of mice exposed to an enriched environment compared with littermates housed in standard cages. We also show, using unbiased stereology, that the enriched mice have a larger hippocampal granule cell layer and 15 per cent more granule cell neurons in the dentate gyrus.
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            Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

            Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.
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              Adverse childhood experiences and the risk of depressive disorders in adulthood.

              Research examining the association between childhood abuse and depressive disorders has frequently assessed abuse categorically, thus not permitting discernment of the cumulative impact of multiple types of abuse. As previous research has documented that adverse childhood experiences (ACEs) are highly interrelated, we examined the association between the number of such experiences (ACE score) and the risk of depressive disorders. Retrospective cohort study of 9460 adult health maintenance organization members in a primary care clinic in San Diego, CA who completed a survey addressing a variety of health-related concerns, which included standardized assessments of lifetime and recent depressive disorders, childhood abuse and household dysfunction. Lifetime prevalence of depressive disorders was 23%. Childhood emotional abuse increased risk for lifetime depressive disorders, with adjusted odds ratios (ORs) of 2.7 [95% confidence interval (CI), 2.3-3.2] in women and 2.5 (95% CI, 1.9-3.2) in men. We found a strong, dose-response relationship between the ACE score and the probability of lifetime and recent depressive disorders (P<0.0001). This relationship was attenuated slightly when a history of growing up with a mentally ill household member was included in the model, but remained significant (P<0.001). The number of ACEs has a graded relationship to both lifetime and recent depressive disorders. These results suggest that exposure to ACEs is associated with increased risk of depressive disorders up to decades after their occurrence. Early recognition of childhood abuse and appropriate intervention may thus play an important role in the prevention of depressive disorders throughout the life span.
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                Author and article information

                Journal
                European Archives of Psychiatry and Clinical Neuroscience
                Eur Arch Psychiatry Clin Neurosci
                Springer Science and Business Media LLC
                0940-1334
                1433-8491
                April 2006
                November 29 2005
                April 2006
                : 256
                : 3
                : 174-186
                Article
                10.1007/s00406-005-0624-4
                3232061
                16311898
                095158d7-2317-4242-9a5e-e8f5bd58ef3d
                © 2006

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