scholarly journals Childhood adversity predicts reduced physiological flexibility during the processing of negative affect among adolescents with major depression histories

2017 ◽  
Vol 121 ◽  
pp. 22-28 ◽  
Author(s):  
Shimrit Daches ◽  
Maria Kovacs ◽  
Charles J. George ◽  
Ilya Yaroslavsky ◽  
Eniko Kiss ◽  
...  
2019 ◽  
Author(s):  
Lotta-Katrin Pries ◽  
Boris Klingenberg ◽  
Claudia Menne-Lothmann ◽  
Jeroen Decoster ◽  
Ruud van Winkel ◽  
...  

AbstractBackgroundThe earliest stages of the pluripotent psychopathology on the pathway to psychotic disorders is represented by emotional dysregulation and subtle psychosis expression, which can be measured using the Ecological Momentary Assessment (EMA). However, it is not clear to what degree common genetic and environmental risk factors for psychosis contribute to variation in these early expressions of psychopathology.MethodsIn this largest ever EMA study of a general population twin cohort including 593 adolescents and young adults between the ages of 15 and 35 years, we tested whether polygenic risk score for schizophrenia (PRS-S) interacts with childhood adversity (the Childhood Trauma Questionnaire score) and daily-life stressors to influence momentary mental state domains (negative affect, positive affect, and subtle psychosis expression) and stress-sensitivity measures.ResultsBoth childhood adversity and daily-life stressors were associated with increased negative affect, decreased positive affect, and increased subtle psychosis expression, while PRS-S was only associated with increased positive affect. No gene–environment correlation was detected. We have provided novel evidence for interaction effects between PRS-S and childhood adversity to influence momentary mental states [negative affect (b = 0.07, 95% CI 0.01 to 0.13, P = 0.013), positive affect (b = −0.05, 95% CI −0.10 to −0.00, P = 0.043), and subtle psychosis expression (b = 0.11, 95% CI 0.03 to 0.19, P = 0.007)] and stress-sensitivity measures.ConclusionExposure to childhood adversities, particularly in individuals with high PRS-S, is pleiotropically associated with emotional dysregulation and psychosis proneness.


2017 ◽  
Vol 46 (3) ◽  
pp. 292-301 ◽  
Author(s):  
Katherine Berry ◽  
Paul Fleming ◽  
Samantha Wong ◽  
Sandra Bucci

Background: Childhood adversity, dissociation and adult attachment have all been implicated in the development of hallucinations or ‘voice-hearing’. Testing psychological models in relation to subclinical phenomena, such as proneness to hallucinations in non-clinical samples, provides a convenient methodology to develop understanding of the processes and mechanisms underlying clinical symptoms. Aims: This paper investigates the relative contribution of childhood adversity, dissociation and adult attachment in explaining hallucination proneness in a non-clinical sample. Methods: Students and staff with no previous contact with secondary care at the University of Manchester were recruited. Participants completed a series of self-report measures: the Launay‒Slade Hallucination Scale (LSHS), the Relationship Scale Questionnaire (RSQ), the Childhood Trauma Questionnaire (CTQ), the Dissociative Experiences Schedule (DES II) and the Positive and Negative Affect Schedule (PANAS). Results: As hypothesized, insecure attachment, childhood adversity and dissociative symptoms were correlated with hallucination proneness. Multiple regression analysis, controlling for confounds of age and negative affect, indicated that the RSQ, CTQ and DES II predicted hallucination proneness. Only DES II and RSQ avoidant attachment were significant independent predictors in the final model. Conclusions: This study provides further evidence to support the idea that attachment and dissociation are important psychological mechanisms involved in voice-hearing proneness. Further testing is required with a clinical population.


2004 ◽  
Vol 34 (8) ◽  
pp. 1465-1474 ◽  
Author(s):  
RENEE D. GOODWIN ◽  
DAVID M. FERGUSSON ◽  
L. JOHN HORWOOD

Background. The objectives of the study were to examine linkages between asthma and depressive and anxiety disorders in a birth cohort of over 1000 young persons studied to the age of 21 years. Specifically, the study aimed to ascertain the extent to which associations between asthma and depressive and anxiety disorders could be explained by non-observed fixed confounding factors.Method. Asthma and depressive and anxiety disorders were measured prospectively over the course of a 21-year longitudinal study. Fixed effects logistic regression models were used to determine the relationship between asthma and depressive and anxiety disorders, adjusting for potentially confounding factors.Results. Asthma in adolescence and young adulthood was associated with increased likelihood of major depression (OR 1·7, 95% CI 1·3–2·3), panic attacks (OR 1·9, 95% CI 1·3–2·8), and any anxiety disorder (OR 1·6, 95% CI 1·2–2·2). Associations between asthma and depressive and anxiety disorders were adjusted for confounding factors using a fixed effects regression model which showed that, after control for fixed confounding factors, asthma was no longer significantly related to major depression (OR 1·1), panic attacks (OR 1·1), or any anxiety disorder (OR 1·2). Additional post hoc analyses suggested that exposure to childhood adversity or unexamined familial factors may account for some of the co-morbidity of asthma and depressive and anxiety disorders.Conclusions. These results confirm and extend previous findings by documenting elevated rates of depressive and anxiety disorders among young adults with asthma, compared with their counterparts without asthma, in the community. The weight of the evidence from this study suggests that associations between asthma and depressive and anxiety symptoms may reflect effects of common factors associated with both asthma and depressive and anxiety disorders, rather than a direct causal link. Future research is needed to identify the specific factors underlying these associations.


2017 ◽  
Author(s):  
Mariam M. Youssef ◽  
Mark D. Underwood ◽  
Yung-Yu Huang ◽  
Shu-chi Hsiung ◽  
Yan Liu ◽  
...  

ABSTRACTBrain-derived neurotrophic factor (BDNF) is implicated in the pathophysiology of major depressive disorder (MDD) and suicide. Both are partly caused by early life adversity (ELA) and ELA reduces both BDNF protein and gene expression. This study examines the association of BDNF Val66Met polymorphism and brain BDNF levels with depression and suicide. We hypothesized that both MDD and ELA would be associated with the Met allele and lower brain BDNF levels. Such an association would be consistent with low BDNF mediating the effect of ELA on adulthood suicide and MDD. BDNF Val66Met polymorphism was genotyped in postmortem brains of 37 suicide decedents and 53 non-suicides. Additionally, BDNF protein levels were determined by Western blot in dorsolateral prefrontal cortex (Brodmann area 9; BA9), anterior cingulate cortex (ACC; BA24), caudal brainstem and rostral brainstem. The relationships between these measures and major depression, death by suicide and reported childhood adversity were examined. Depressed subjects had an excess of the Met allele and lower BDNF levels in ACC and caudal brainstem compared with non-depressed subjects. No effect of history of suicide death or early life adversity was observed with genotype, but lower BDNF levels in ACC were found in subjects who had been exposed to early life adversity and/or died by suicide compared to nonsuicide decedents and no reported childhood adversity. This study provides further evidence for low BDNF in major depression related to the BDNF met risk allele. Future studies should seek to determine how altered BDNF expression contributes to MDD and suicide.


2018 ◽  
Vol 83 (9) ◽  
pp. S409-S410
Author(s):  
Andre Do ◽  
Tamara Cassis ◽  
Pablo Cervantes ◽  
Marie Saint Laurent ◽  
Nancy Low

2017 ◽  
Vol 83 ◽  
pp. 42
Author(s):  
Michael Kaczmarczyk ◽  
Katja Wingenfeld ◽  
Linn Kuehl ◽  
Christian Otte ◽  
Kim Hinkelmann

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