Stress load during childhood affects psychopathology in psychiatric patients

Department of Psychology, University of Konstanz, Germany.
BMC Psychiatry (Impact Factor: 2.21). 07/2008; 8(1):63. DOI: 10.1186/1471-244X-8-63
Source: PubMed


Childhood stress and trauma have been related to adult psychopathology in different psychiatric disorders. The present study aimed at verifying this relationship for stressful experiences during developmental periods by screening stress load across life in adult psychiatric inpatients with different diagnoses compared to healthy subjects. In addition, a relationship between the amount of adverse experiences and the severity of pathology, which has been described as a 'building block' effect in posttraumatic stress disorder (PTSD), was explored for non-traumatic events in psychiatric disorders other than PTSD.
96 patients with diagnoses of Major Depressive Disorder (MDD), schizophrenia, drug addiction, or personality disorders (PD) and 31 subjects without psychiatric diagnosis were screened for adverse experiences in childhood (before the age of six years), before onset of puberty, and in adulthood using the Early Trauma Inventory and the Posttraumatic Stress Diagnostic Scale. Effects of stress load on psychopathology were examined for affective symptoms, PTSD, and severity of illness by regression analyses and comparison of subgroups with high and low stress load.
High stress load in childhood and before puberty, but not in adulthood, was related to negative affect in all participants. In patients, high stress load was related to depressive and posttraumatic symptoms, severity of disorder, and the diagnoses of MDD and PD.
Results support the hypothesis of stress-sensitive periods during development, which may interact with genetic and other vulnerability factors in their influence on the progress of psychiatric disorders. A 'dose' effect of stress load on the severity of psychopathology is not restricted to the relationship between traumata and PTSD.

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    • "Early life stress (ELS) has shown to have profound impacts on health throughout the lifespan (Alastalo et al., 2013; Etter et al., 2013; MacMillan et al., 2001) and it can induce changes on behavioral and metabolic responses later in life (Pervanidou and Chrousos, 2012). Studies have shown that ELS is associated with depression, personality disorders (Sudbrack et al., 2015; Weber et al., 2008), temperament traits (Sudbrack et al., 2015), anxiety, drug addiction and antisocial behavior in adulthood (MacMillan et al., 2001) as well as a variety of other medical problems (Fergusson et al., 2008; Spitzer et al., 2013). Among the different types of trauma, physical abuse is consistently associated with poor outcomes (Bailer et al., 2014; Bailey et al., 2012; Fuller-Thomson and Hooper, 2015; Petrenko et al., 2012; Schneiderman et al., 2014). "
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    ABSTRACT: An adverse early life environment can induce changes on behavioral and metabolic responses later in life. Recent studies in rats showed that the quality of maternal care as measured by high levels of pup licking and grooming (LG) was associated with changes in the relationship between the precursor thyroid-hormone T4 and the more active T3. Here we investigated if early exposure to childhood abuse is associated with thyroid-hormone levels in human adolescents. Given the empirical evidence from animal models showing that good maternal care was associated with increased conversion of T4 to T3, we hypothesized that early adversity would be associated with a decreased peripheral conversion of T4 to T3. A sample of 80 adolescents (10–18 years) participated in this study. We used the Childhood Trauma Questionnaire to investigate early life stress. We calculate the body mass index (BMI) assessing weight and height and sexual maturation stage was determined by self-assessment. Blood samples were collected to measure T3 and T4 levels. ANCOVA were used to evaluate the influence of the Physical Abuse domain of the Childhood Trauma Questionnaire as the early life stress variable in T3 and T4 separately, adjusted for potential confounders such as pubertal status, gender, socioeconomic status and BMI. Early life trauma was associated with reduced T3 levels in adolescents, when adjusted for potential confounders (p = 0.013), but not with peripheral T4 levels (p = 0.625). We extended findings from animal models showing that adverse early experience persistently impacts on the individual's responses to stress, which is marked by an abnormal metabolism of thyroid hormones. Further studies are needed to further investigate the nature of such associations.
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    • "A growing number of studies indicate that adverse early life experiences may be an important factor in the pathogenesis of depression , due to effects on neurodevelopment ( Teicher et al . , 2003 ; de Kloet et al . , 2005 ; Weber et al . , 2008 ) . The molecular mechanisms underlying these changes are an active area of investigation . It has been postulated that stressful events during critical periods of development influence brain by affecting the nervous , endocrine and immune systems . Recent data has shown that changes in the intrauterine environment during the prenatal p"
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    ABSTRACT: Several lines of evidence suggest that the dysregulation of the immune system is an important factor in the development of depression. Microglia are the resident macrophages of the central nervous system and a key player in innate immunity of the brain. We hypothesized that prenatal stress (an animal model of depression) as a priming factor could affect microglial cells and might lead to depressive-like disturbances in adult male rat offspring. We investigated the behavioral changes (sucrose preference test, Porsolt test), the expression of C1q and CD40 mRNA and the level of microglia (Iba1 positive) in 3 month old control and prenatally stressed male offspring rats. In addition, we characterized the morphological and biochemical parameters of potentially harmful (NO, iNOS, IL-1β, IL-18, IL-6, TNF-α, CCL2, CXCL12, CCR2, CXCR4) and beneficial (IGF-1, BDNF) phenotypes in cultures of microglia obtained from the cortices of 1-2 days old control and prenatally stressed pups. The adult prenatally stressed rats showed behavioral (anhedonic- and depression-like) disturbances, enhanced expression of microglial activation markers and an increased number of Iba1-immunopositive cells in the hippocampus and frontal cortex. The morphology of glia was altered in cultures from prenatally stressed rats, as demonstrated by immunofluorescence microscopy. Moreover, in these cultures, we observed enhanced expression of CD40 and MHC II and release of pro-inflammatory cytokines, including IL-1β, IL-18, TNF-α and IL-6. Prenatal stress significantly up-regulated levels of the chemokines CCL2, CXCL12 and altered expression of their receptors, CCR2 and CXCR4 while IGF-1 production was suppressed in cultures of microglia from prenatally stressed rats. Our results suggest that prenatal stress may lead to excessive microglia activation and contribute to the behavioral changes observed in depression in adulthood.
    Frontiers in Cellular Neuroscience 03/2015; 9. DOI:10.3389/fncel.2015.00082 · 4.29 Impact Factor
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    • "Alexithymia, defined as the difficulty identifying, decoding, and communicating one's own emotional state (Franz et al., 2008), has been described as one potential outcome of ELS on the behavioral level (Freyberger, 1977; Frewen et al., 2008; Lumley et al., 2007). Its association with ELS has been demonstrated in a number of clinical studies (e.g., Weber et al., 2008; Wingenfeld et al., 2011) and also in a very recent investigation of healthy individuals (Aust et al., 2013a). On the neural level, alexithymia has been linked to reduced limbic responses to emotional stimuli (e.g., in the amygdala, Kugel et al., 2008; for a recent review, see Moriguchi and Komaki, 2013). "
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    ABSTRACT: Early life stress (ELS) is known to have considerable influence on brain development and affective functioning. Previous studies in clinical populations have shown that hippocampus and amygdala, two central structures of limbic emotion processing circuits, are predominantly affected by early stress exposure. Given the inconsistent findings on ELS-related effects in healthy populations and the associations of ELS and affective functioning, the question arises which additional emotion-relevant variables need to be considered to better understand the effects of ELS. We therefore investigated the volume of hippocampus and amygdala in 25 high alexithymic (h-ALEX) and 25 low alexithymic (l-ALEX) individuals, which were matched with regard to ELS, but significantly differed in their degree of emotional functioning. Volumetric analyses were performed using FSL-FIRST, a method to automatically segment subcortical structures on T1-weighted magnetic resonance images. Alexithymia was assessed using the Toronto Alexithymia Scale and Bermond-Vorst Alexithymia Questionnaire. ELS was assessed by Childhood Trauma Questionnaire (CTQ) and Early Trauma Inventory. Our data showed that ELS was negatively associated with right hippocampus volume in h-ALEX individuals, while there was no such association in the l-ALEX group. Furthermore, ELS was positively associated with left amygdala volume in l-ALEX individuals, but not in individuals with high levels of alexithymia. The present study emphasizes a substantial relationship between intrapersonal factors such as alexithymia and neural alterations related to the experience of ELS. Longitudinal study designs are necessary to pursue the question of how emotional abilities interact with individual adaptations to early stress exposure on the neural level. © 2014 Wiley Periodicals, Inc.
    Hippocampus 09/2014; 24(9). DOI:10.1002/hipo.22293 · 4.16 Impact Factor
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