Association between childhood trauma and catecholamine response to psychological stress in police academy recruits.

BACKGROUND: Childhood trauma is a risk factor for anxiety disorders in adulthood. One possible mechanism for this association is an increased neuroendocrine response to stress in adults with a history of childhood trauma. METHODS: In a cross-sectional study, 76 police academy recruits (mean [+/-SD] age 28 +/- 5 years, 10 female) were exposed to a video depicting real-life officers exposed to highly stressful incidents. Salivary cortisol and 3-methoxy-4-hydroxy-phenylglycol (MHPG, the major metabolite of norepinephrine) were collected at baseline, immediately after the video, and 20 min after the video. Childhood trauma before age 14 was assessed with an interview (Life Stressor Checklist-Revised). RESULTS: Exposure to the video elicited significant MHPG and cortisol responses in both groups. Recruits with childhood trauma histories (n = 16) had a significantly greater MHPG response, as evidenced by a group effect (F = 8.0, p < .01), and a group x time interaction (F = 4.1, p < .05). The cortisol response did not differ between groups. CONCLUSIONS: Police academy recruits with childhood trauma histories have an increased catecholamine response to psychological stress. This might serve as a risk factor for anxiety disorders in recruits, and these findings might generalize to other groups with a history of childhood trauma.     

Pituitary-adrenal responses to standard and low-dose dexamethasone suppression tests in adult survivors of child abuse.

BACKGROUND: Previous studies indicate that adverse childhood events are associated with persistent changes in corticotropin-releasing factor neuronal systems. Our aim was to determine whether altered glucocorticoid feedback mediates the neuroendocrine sequelae of childhood trauma. METHODS: Standard and low-dose dexamethasone suppression tests (DST) were performed in women with a history of child abuse (n=19), child abuse and major depression (n=16), major depression and no childhood trauma (n=10), and no history of mental illness or childhood trauma (n=19). Secondary analysis with posttraumatic stress disorder (PTSD) as the organizing diagnosis was also conducted. RESULTS: In the low-dose DST, depressed women with a history of abuse exhibited greater cortisol suppression than any comparator group and greater corticotropin suppression than healthy volunteers or nondepressed abuse survivors. There were no differences between nondepressed abuse survivors and healthy volunteers in the low-dose DST or between any subject groups in the standard DST. The PTSD analysis produced similar results. CONCLUSIONS: Cortisol supersuppression is evident in psychiatrically ill trauma survivors, but not in nondepressed abuse survivors, indicating that enhanced glucocorticoid feedback is not an invariable consequence of childhood trauma but is more related to the resultant psychiatric illness in traumatized individuals.     

Early adverse experience and risk for chronic fatigue syndrome: results from a population-based study

CONTEXT: Chronic fatigue syndrome (CFS) is an important public health problem. The causes of CFS are unknown and effective prevention strategies remain elusive. A growing literature suggests that early adverse experience increases the risk for a range of negative health outcomes, including fatiguing illnesses. Identification of developmental risk factors for CFS is critical to inform pathophysiological research and devise targets for primary prevention. OBJECTIVE: To examine the relationship between early adverse experience and risk for CFS in a population-based sample of clinically confirmed CFS cases and nonfatigued control subjects. DESIGN, SETTING, AND PARTICIPANTS: A case-control study of 43 cases with current CFS and 60 nonfatigued controls identified from a general population sample of 56 146 adult residents from Wichita, Kan. MAIN OUTCOME MEASURES: Self-reported childhood trauma (sexual, physical, and emotional abuse and emotional and physical neglect) and psychopathology (depression, anxiety, and posttraumatic stress disorder) by CFS status. RESULTS: The CFS cases reported significantly higher levels of childhood trauma and psychopathology compared with the controls. Exposure to childhood trauma was associated with a 3- to 8-fold increased risk for CFS across different trauma types. There was a graded relationship between the degree of trauma exposure and CFS risk. Childhood trauma was associated with greater CFS symptom severity and with symptoms of depression, anxiety, and posttraumatic stress disorder. The risk for CFS conveyed by childhood trauma increased with the presence of concurrent psychopathology. CONCLUSIONS: This study provides evidence of increased levels of multiple types of childhood trauma in a population-based sample of clinically confirmed CFS cases compared with nonfatigued controls. Our results suggest that childhood trauma is an important risk factor for CFS. This risk was in part associated with altered emotional state. Studies scrutinizing the psychological and neurobiological mechanisms that translate childhood adversity into CFS risk may provide direct targets for the early prevention of CFS.     

The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: a multiple regression analysis

Sensitization of stress-responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood.     

Childhood trauma and psychosis - what is the evidence?

In the last decade, a substantial number of population-based studies have suggested that childhood trauma is a risk factor for psychosis. In several studies, the effects held after adjusting for a wide range of potentially confounding variables, including genetic liability for psychosis. Less is known about the mechanisms underlying the association between childhood trauma and psychosis. Possible pathways include relationships between negative perceptions of the self, negative affect, and psychotic symptoms, as well as biological mechanisms such as dysregulated cortisol and increased sensitivity to stress. Psychotic patients with a history of childhood trauma tend to present with a variety of additional problems, including post-traumatic stress disorder, greater substance abuse, higher levels of depression and anxiety, and more frequent suicide attempts. Initial studies suggest that trauma-specific treatments are as beneficial for these patients as for other diagnostic groups.     

Childhood trauma history differentiates amygdala response to sad faces within MDD

Objective

Heightened amygdala reactivity to aversive stimuli in major depression is regarded as a core feature of the underlying physiology but individual differences in amygdala response may also arise secondary to persistent changes in limbic function during early neurodevelopment relative to stressors such as childhood trauma. We sought to determine whether heightened amygdala response is a core feature of depression or a general risk factor for psychopathology secondary to early life stress.

Method

Twenty unipolar depressed patients with and without a history of significant early life trauma and 16 healthy comparison subjects underwent functional MRI in a cross-sectional study comparing neural response to sad and neutral faces.

Results

We observed a robust positive correlation between physical abuse and right amygdala response. A much weaker relationship with other forms of abuse and neglect was also found, suggesting differences between abuse subtypes and amygdala response. Group differences in amygdala response suggest heightened reactivity was not characteristic of persons with depression in general but was true primarily in those with a significant history of abuse.

Conclusion

These findings suggest the relationship between childhood trauma and risk for depression is mediated by heightened amygdala response but varies by abuse type. Preliminary evidence for two distinct depression phenotypes based on trauma history was also supported, consistent with differential etiology.     

Childhood trauma and diurnal cortisol disruption in fibromyalgia syndrome

Adults with fibromyalgia syndrome report high rates of childhood trauma. Neuroendocrine abnormalities have also been noted in this population. Exploratory analyses tested relationships between retrospective reports of childhood trauma and diurnal salivary cortisol patterns among 85 women with fibromyalgia. Subjects with fibromyalgia completed self-reports of childhood physical, sexual and emotional abuse, as well as emotional and physical neglect. Recent major life events, current perceptions of stress, and depressive symptoms were also assessed. Salivary cortisol was collected six times per day for two consecutive days to assess diurnal rhythm, awakening response and mean cortisol levels. Hierarchical regression analyses were performed, controlling for age, relevant medications, life events, perceived stress, and depressive symptoms. Childhood physical abuse predicted flattened diurnal cortisol rhythms as well as greater cortisol responses to awakening. Sexual abuse was a second predictor of increased awakening cortisol responses. Patients with a history of trauma had markedly low levels of cortisol at the time of first awakening, partly explaining the results. These findings suggest that severe traumatic experiences in childhood may be a factor of adult neuroendocrine dysregulation among fibromyalgia sufferers. Trauma history should be evaluated and psychosocial intervention may be indicated as a component of treatment for fibromyalgia.     

Childhood trauma,HPA axis activity and antidepressant response in patients with depression

Childhood trauma is among the most potent contributing risk factors for depression and is associated with poor treatment response. Hypothalamic-pituitary-adrenal (HPA) axis abnormalities have been linked to both childhood trauma and depression, but the underlying mechanisms are poorly understood. The present study aimed to investigate the link between childhood trauma, HPA axis activity and antidepressant response in patients with depression. As part of the Wellcome Trust NIMA consortium, 163 depressed patients and 55 healthy volunteers were included in this study. Adult patients meeting Structured Clinical Interview for Diagnostic and Statistical Manual Version-5 criteria for major depression were categorised into subgroups of treatment responder (n = 42), treatment non-responder (n = 80) and untreated depressed (n = 41) based on current depressive symptom severity measured by the 17-item Hamilton Rating Scale for Depression and exposure to antidepressant medications established by Antidepressant Treatment Response Questionnaire. Childhood Trauma Questionnaire was obtained. Baseline serum C-reactive protein was measured using turbidimetric detection. Salivary cortisol was analyzed at multiple time points during the day using the ELISA technique. Glucocorticoid resistance was defined as the coexistence of hypercortisolemia and inflammation. Our results show that treatment non-responder patients had higher exposure to childhood trauma than responders. No specific HPA axis abnormalities were found in treatment non-responder depressed patients. Untreated depressed showed increased diurnal cortisol levels compared with patients on antidepressant medication, and higher prevalence of glucocorticoid resistance than medicated patients and controls. The severity of childhood trauma was associated with increased diurnal cortisol levels only in individuals with glucocorticoid resistance. Therefore, our findings suggest that the severity of childhood trauma experience contributes to a lack of response to antidepressant treatment. The effects of childhood trauma on increased cortisol levels are specifically evident in patients with glucocorticoid resistance and suggest glucocorticoid resistance as a target for the development of personalized treatment for a subgroup of depressed patients with a history of childhood trauma rather than for all patients with resistance to antidepressant treatment.     

Stress and development of depression and heavy drinking in adulthood: moderating effects of childhood trauma

Purpose

Studies suggest that childhood trauma is linked to both depression and heavy drinking in adulthood, and may create a lifelong vulnerability to stress. Few studies have explored the effects of stress sensitization on the development of depression or heavy drinking among those who have experienced traumatic childhood events. This study aimed to determine the effect of childhood trauma on the odds of experiencing depression or heavy drinking in the face of an adult life stressor, using a large population-based Canadian cohort.

Methods

A total of 3,930 participants were included from the National Population Health Survey. The associations among childhood trauma, recent stress and depression/heavy drinking from 1994/1995 to 2008/2009 were explored using logistic regression, as were interactions between childhood trauma and recent stress. A generalized linear mixed model was used to determine the effects of childhood trauma and stressful events on depression/heavy drinking. Analyses were stratified by sex.

Results

Childhood trauma significantly increased the odds of becoming depressed (following 1 event: OR = 1.66; 95 %CI 1.01, 2.71; 2+ events, OR = 3.89; 95 %CI 2.44, 6.22) and drinking heavily (2+ events: OR = 1.79; 95 %CI 1.03, 3.13). Recent stressful events were associated with depression, but not heavy drinking. While most interaction terms were not significant, in 2004/2005 the association between recent stress and depression was stronger in those who reported childhood trauma compared to those with no childhood trauma.

Conclusions

Childhood trauma increases risk for both depression and heavy drinking. Trauma may moderate the effect of stress on depression; the relationship among trauma, stress and heavy drinking is less clear.     

Psychological trauma,posttraumatic stress disorder and trauma-related depression: A mini-review

There are various types of traumatic stimuli, such as catastrophic events like wars, natural calamities like earthquakes, and personal trauma from physical and psychological neglect or abuse and sexual abuse. Traumatic events can be divided into type I and type II trauma, and their impacts on individuals depend not only on the severity and duration of the traumas but also on individuals’ self-evaluation of the traumatic events. Individual stress reactions to trauma include posttraumatic stress disorder (PTSD), complex PTSD and trauma-related depression. Trauma-related depression is a reactive depression with unclear pathology, and depression occurring due to trauma in the childhood has gained increasing attention, because it has persisted for a long time and does not respond to conventional antidepressants but shows good or partial response to psychotherapy, which is similar to the pattern observed for PTSD. Because trauma-related depression is associated with high risk of suicide and is chronic with a propensity to relapse, it is necessary to explore its pathogenesis and therapeutic strategy.     

Childhood maltreatment is associated with depression but not with hypochondriasis in later life

Objective

Previous studies demonstrated that a history of childhood trauma is linked to mental disorders in adulthood, particularly to depression. Adverse childhood experiences are also considered to contribute to the risk of hypochondriasis, but the results of previous studies have not been conclusive with respect to the strength and specificity of this association. Therefore, we compared the association of adverse childhood experiences with both hypochondriasis and depression.

Methods

Fifty-eight patients with hypochondriasis, 52 patients with depression, and 52 healthy control participants completed the Childhood Trauma Questionnaire (CTQ) which assesses 5 varieties of abuse and neglect. A clinical interview (SCID-I) was used to establish DSM-IV diagnoses. Associations between childhood maltreatment, hypochondriasis and depression were estimated by means of analyses of variance and multiple linear regression analyses.

Results

In comparison to hypochondriacal and healthy participants, patients with a current depressive disorder reported more emotional abuse as well as more emotional and physical neglect during childhood. Patients with hypochondriasis reported more emotional neglect than healthy individuals. However, when predicting the CTQ trauma types by diagnostic category adjusting for sex and comorbid DSM-IV diagnoses, emotional abuse, emotional neglect, physical abuse, physical neglect, as well as the CTQ total score were significantly associated with depression, but none of the CTQ scores was significantly related to hypochondriasis.

Conclusions

The findings suggest a robust association of childhood maltreatment with depression but not with hypochondriasis. This result does not support etiological models of hypochondriasis which rely on childhood maltreatment as a risk factor for the development of this disorder.     

Is impulsivity a link between childhood abuse and suicide?

Childhood abuse and neglect are known to affect psychological states through behavioral, emotional, and cognitive pathways. They increase the risk of having psychiatric diseases in adulthood and have been considered risk factors for suicidal behavior in all diagnostic categories. Early, prolonged, and severe trauma is also known to increase impulsivity, diminishing the capacity of the brain to inhibit negative actions and to control and modulate emotions. Many neurobiological studies hold that childhood maltreatment may lead to a persistent failure of the inhibitory processes ruled mainly by the frontal cortex over a fear-motivated hyperresponsive limbic system. Multiple neurotransmitters and hormones are involved in the stress response, but, to our knowledge, the two major biological consequences of the chronic exposure to trauma are the hypofunction of the serotonergic system and changes in the hypothalamic-pituitary-adrenal axis function. Some of these findings overlap with the neurobiological features of impulsivity and of suicidal behavior. Impulsivity has also been said to be both a consequence of trauma and a risk factor for the development of a pathological response to trauma. Thus, we suggest that impulsivity could be one of the links between childhood trauma and suicidal behavior. Prevention of childhood abuse could significantly reduce suicidal behavior in adolescents and adults, in part, through a decrease in the frequency of impulsive behaviors in the future.     

Childhood abuse is associated with increased startle reactivity in adulthood

Background: Understanding the neurobiological correlates of childhood maltreatment is critical to delineating stress‐related psychopathology. The acoustic startle response (ASR) is a subcortical reflex modulated by neural systems implicated in posttraumatic stress disorder (PTSD). The ASR is conserved across species and is increased in rodent models of developmental stress. Methods: We measured ASR to a 40 ms noise probe as well as fear‐potentiated startle using electromyographic recordings of the eyeblink in a primarily African American sample (N=60) from a highly traumatized civilian population. We assessed self‐reported history of abuse with the Childhood Trauma Questionnaire and current symptoms with the PTSD Symptom Scale and the Beck Depression Inventory. Results: We found that subjects reporting a history of high levels of physical or sexual abuse had increased startle on all trial types relative to those with low abuse (P<.01). This effect remained significant after co‐varying for the subjects' age and sex, as well as PTSD and depression symptoms. Perceived childhood sexual abuse was the greatest predictor of increased startle response. Notably, emotional abuse in childhood did not affect baseline startle, and all groups demonstrated equivalent levels of fear‐potentiated startle. Conclusions: The long‐lasting effects of early life trauma result in increased risk for adult psychopathology. These new data demonstrate that a self‐report history of child abuse is related to altered baseline startle response that is not accounted for by PTSD or depression symptoms. Increased startle may be a biomarker of stress responsiveness that can be a persevering consequence of early trauma exposure during childhood. Depression and Anxiety 26:1018–1026, 2009. Published 2009 Wiley‐Liss, Inc.     

Do Child Abuse and Maltreatment Increase Risk of Schizophrenia?

Introduction

IntroductionaaAlthough childhood abuse is a recognised risk factor for depression, post-traumatic stress disorder, and substance misuse, its role in the aetiology of psychotic disorder remained controversial. This is in part because the putative effect of childhood trauma on psychosis has been mostly evaluated by small, cross sectional, uncontrolled studies that raised methodological issues.

Methods

Papers concerning the association between childhood trauma and psychotic disorders (to November, 2011) were identified using a comprehensive search of PubMed, Psychinfo, and Scopus and analysing reference list of relevant papers. A narrative synthesis was used to summarise results.

Results

An association between childhood abuse and psychotic symptoms was consistently reported by large cross sectional surveys with an effect ranging from 1.7 to 15. However, we cannot conclude that the relationship is causal as lack of longitudinal studies prevent us from fully excluding alternative explanations such as reverse causality. Gender, cannabis use, and depressive and post-traumatic stress disorder symptoms appear to moderate the effect of childhood trauma on psychotic disorders. However, specificity of childhood abuse in psychotic disorders and, particularly, in schizophrenia has not been demonstrated.

Conclusion

Although the association between childhood abuse and psychosis has been replicated, the etiological role of such early adversity has yet to be fully clarified. So far none of the studies reported support the hypothesis that childhood abuse is either sufficient or necessary to develop a psychotic disorder. It seems likely that any effect of childhood abuse on schizophrenia needs to be understood in terms of genetic susceptibility and interaction with other environmental risk factors.     

Childhood trauma in patients with self-reported stress-precipitated seizures

ObjectiveStress is the most commonly reported precipitant of epileptic seizures, but the mechanism by which stress precipitates seizures and the risk factors for stress as a seizure precipitant are poorly understood. Previously, we observed higher levels of anxiety symptoms in patients with epilepsy who reported stress as a seizure precipitant. Given that childhood trauma increases the risk of general psychiatric symptom burden, including anxiety symptoms, we sought to examine the relationship between childhood adversity and stress as a seizure precipitant.MethodsSequential outpatients (N = 236) evaluated at the Epilepsy Center of the University of Cincinnati Neuroscience Institute who had previously enrolled in an earlier study of stress and seizures were enrolled. Subjects either endorsed stress as a seizure precipitant [Stress (+)] or not [Stress (−)]. The Childhood Trauma Questionnaire Short Form (CTQ-SF), a 28-question scale that evaluates 5 domains of childhood adversity (physical abuse, physical neglect, emotional abuse, emotional neglect, and sexual abuse) was sent via mail and returned on paper or electronically from participants. Total CTQ-SF score and CTQ-SF domain scores were compared between Stress (+) and Stress (−) groups using Wilcoxon rank sum test. Spearman's rank correlation between CTQ-SF scores with depression and anxiety was also determined, and these analyses were followed by a multivariate analysis to identify the association of childhood trauma with other factors including anxiety and depression.ResultsA total of 119 out of 236 CTQ-SFs that were sent out were completed. Response rates were 91/195 for Stress (+) and 28/41 for Stress (−). The Stress (+) group reported higher scores in emotional abuse compared with the Stress (−) group (p = 0.029); CTQ-SF total scores were higher in the Stress (+) group compared with the Stress (−) group (p = 0.08), and sexual abuse scores were higher in Stress (+) group (p = 0.07), but there were no statistically significant differences for other types of trauma. Depression and anxiety scores were higher in the Stress (+) group, but anxiety was the only independent factor associated with the Stress (+) group in the multivariate analysis (p = 0.0021).ConclusionPatients with epilepsy who report stress as a seizure precipitant are more likely to endorse a history of childhood traumatic experiences, particularly emotional abuse, compared with those who do not perceive stress as a precipitant. Further study is needed to identify how childhood trauma interacts with anxiety in modulating stress response in patients with epilepsy.     

Childhood reactions to terrorism-induced trauma: a review of the past 10 years

OBJECTIVE: To summarize the literature about the clinical presentation and treatment interventions of childhood reactions to terrorism-induced trauma. METHOD: The literature on children's responses to terrorist activities was reviewed. RESULTS: Over the past 10 years, more research has emerged on the subject of terrorism in children. Many of the effects of terrorism-induced trauma are similar to the effects of natural and man-made trauma. Children's responses include acute stress disorder, posttraumatic stress disorder, anxiety, depression, regressive behaviors, separation problems, sleep difficulties, and behavioral problems. However, several aspects of terrorist attacks result in unique stressors and reactions and pose specific challenges for treatment. The unpredictable, indefinite threat of terrorist events, the profound effect on adults and communities, and the effect of extensive terrorist-related media coverage exacerbates underlying anxieties and contributes to a continuous state of stress and anxiety. Intervention strategies include early community-based interventions, screening of children at risk, triage and referral, and trauma-loss-focused treatment programs. CONCLUSIONS: Advances have been made in the research of childhood reactions to terrorism-induced trauma. Further research is needed to identify children at risk and to determine the long-term impact on children's development. Although the preliminary results of interventions developed to help children are promising, outcome data have not been examined, and further research is needed to evaluate their effectiveness.     

PTSD and the HPA axis: differences in response to the cold pressor task among individuals with child vs. adult trauma

Hypothalamic pituitary adrenal (HPA) axis and subjective stress response to a cold-water immersion task, the cold pressor task (CPT), in individuals (N=89) with post-traumatic stress disorder (PTSD) were examined. All tests were conducted at 08:00h after an overnight hospital stay. Plasma adrenocorticotrophin hormone (ACTH), cortisol, and subjective stress were examined at baseline and five post-task time points in controls (n=31), subjects with PTSD as a result of an index trauma during childhood (i.e. before age 18; n=25), and subjects with PTSD as a result of an index trauma as an adult (n=33). Approximately, 50% of individuals in both trauma groups were alcohol dependent, and the impact of this comorbidity was also examined. Subjects with PTSD, regardless of age of index trauma, had a less robust ACTH response as compared to controls. Regardless of the presence or absence of comorbid alcohol dependence, subjects with childhood trauma had lower cortisol at baseline and at all post-task measurement points and did not demonstrate the decrease in cortisol over the course of the 2h monitoring period seen in subjects with adult index trauma and controls. The findings reveal differences in the neuroendocrine response to the CPT in individuals with PTSD compared to control subjects, and differences in PTSD subjects when examined by age of index trauma.     

Linking the neuroendocrinology of post-traumatic stress disorder with recent neuroanatomic findings.

It has been hypothesized that stress damages the hippocampus and results in myriad other deleterious consequences owing to the toxic effects of cortisol, presumed to be released in excess in response to traumatic stress. Several studies have now demonstrated that hippocampal volumes of trauma survivors with post-traumatic stress disorder (PTSD) are reduced compared to those of nontraumatized persons. Interestingly, however, there is little evidence of increased cortisol release in either the acute or chronic aftermath of stress in trauma survivors who develop this disorder, raising questions about the etiology of the smaller hippocampal volumes as well as the relationship between the neuroendocrine and neuroanatomic alterations in PTSD. This article will review hypothalamic-pituitary-adrenal alterations in PTSD in an attempt to link the neuroendocrine findings with the observation of reduced hippocampal volume. It will be argued that the resolution of the neuroendocrine and neuroanatomic alterations in PTSD depends on understanding the pivotal role of glucocorticoids and their action at glucocorticoid receptors at target brain areas in response to stress and in PTSD.     

Beyond genetics: childhood affective trauma in bipolar disorder

Objectives: Despite the demonstrated high heritability of bipolar disorder, few susceptibility genes have been identified and linkage and/or association studies have produced conflicting results. This search for susceptibility genes is hampered by several methodological limitations, and environmental risk factors for the disease (requiring incorporation into analyses) remain misunderstood. Among them, childhood trauma is probably the most promising environmental factor for further investigation. The objectives are to review the arguments in favor of an association between childhood trauma and bipolar disorder and to discuss the interpretations of such an observation. Methods: We computed a literature search using PubMed to identify relevant publications concerning childhood trauma and bipolar disorder. We also present some personal data in this field. Results: Growing evidence suggests that incidences of childhood trauma are frequent and severe in bipolar disorder, probably affect the clinical expression of the disease in terms of suicidal behavior and age at onset, and also have an insidious influence on the affective functioning of patients between episodes. The relationships between childhood trauma and bipolar disorder suggest several interpretations, mainly a causal link, a neurodevelopmental consequence, or the intergenerational transmission of traumatic experiences. The neurobiological consequences of childhood trauma on a maturing brain remain unclear, although such stressors may alter the organization of brain development, leading to inadequate affective regulation. Conclusions: Childhood trauma is associated with bipolar disorder and its clinical expression and may interact with genetic susceptibility factors. Although not completely understood, the relationships between childhood trauma and bipolar disorder require further attention. Several suggestions for further exploration of this environmental factor and of its interaction with susceptibility genes are proposed.     

The loss of a parent during childhood as a risk factor for depression.

While the loss of a parent during childhood may put a person at risk for depression, many studies have failed to confirm the importance of this risk factor. Nevertheless, the relationship between the loss of a parent and depression is of clinical importance. This paper reviews studies of the loss of a parent as a risk factor for depression. In addition, relevant data from these studies were pooled using meta-analytic techniques. It was found that for females there was a significant association between the loss of one's mother before age 11 and depression, and that losing one's mother during early childhood may double their risk of depression.