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      Network Approach to Understanding Emotion Dynamics in Relation to Childhood Trauma and Genetic Liability to Psychopathology: Replication of a Prospective Experience Sampling Analysis

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          Abstract

          Background: The network analysis of intensive time series data collected using the Experience Sampling Method (ESM) may provide vital information in gaining insight into the link between emotion regulation and vulnerability to psychopathology. The aim of this study was to apply the network approach to investigate whether genetic liability (GL) to psychopathology and childhood trauma (CT) are associated with the network structure of the emotions “cheerful,” “insecure,” “relaxed,” “anxious,” “irritated,” and “down”—collected using the ESM method.

          Methods: Using data from a population-based sample of twin pairs and siblings (704 individuals), we examined whether momentary emotion network structures differed across strata of CT and GL. GL was determined empirically using the level of psychopathology in monozygotic and dizygotic co-twins. Network models were generated using multilevel time-lagged regression analysis and were compared across three strata (low, medium, and high) of CT and GL, respectively. Permutations were utilized to calculate p values and compare regressions coefficients, density, and centrality indices. Regression coefficients were presented as connections, while variables represented the nodes in the network.

          Results: In comparison to the low GL stratum, the high GL stratum had significantly denser overall ( p = 0.018) and negative affect network density ( p < 0.001). The medium GL stratum also showed a directionally similar (in-between high and low GL strata) but statistically inconclusive association with network density. In contrast to GL, the results of the CT analysis were less conclusive, with increased positive affect density ( p = 0.021) and overall density ( p = 0.042) in the high CT stratum compared to the medium CT stratum but not to the low CT stratum. The individual node comparisons across strata of GL and CT yielded only very few significant results, after adjusting for multiple testing.

          Conclusions: The present findings demonstrate that the network approach may have some value in understanding the relation between established risk factors for mental disorders (particularly GL) and the dynamic interplay between emotions. The present finding partially replicates an earlier analysis, suggesting it may be instructive to model negative emotional dynamics as a function of genetic influence.

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          Most cited references34

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          Core affect and the psychological construction of emotion.

          At the heart of emotion, mood, and any other emotionally charged event are states experienced as simply feeling good or bad, energized or enervated. These states--called core affect--influence reflexes, perception, cognition, and behavior and are influenced by many causes internal and external, but people have no direct access to these causal connections. Core affect can therefore be experienced as free-floating (mood) or can be attributed to some cause (and thereby begin an emotional episode). These basic processes spawn a broad framework that includes perception of the core-affect-altering properties of stimuli, motives, empathy, emotional meta-experience, and affect versus emotion regulation; it accounts for prototypical emotional episodes, such as fear and anger, as core affect attributed to something plus various nonemotional processes.
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            Stressful life events, genetic liability, and onset of an episode of major depression in women.

            This study was undertaken to clarify how genetic liability and stressful life events interact in the etiology of major depression. Information about stressful life events and onset of major depressive episodes in the past year was collected in a population-based sample of female-female twin pairs including 2,164 individuals, 53,215 person-months of observation, and 492 onsets of depression. Nine "personal" and three aggregate "network" stressful events significantly predicted onset of major depression in the month of occurrence, four of which predicted onset with an odds ratio of > 10 and were termed "severe": death of a close relative, assault, serious marital problems, and divorce/breakup. Genetic liability also had a significant impact on risk of onset of depression. For severe stressful events, as well as for 10 of the 12 individual stressful events, the best-fitting model for the joint effect of stressful events and genetic liability on onset of major depression suggested genetic control of sensitivity to the depression-inducing effects of stressful life events. In individuals at lowest genetic risk (monozygotic twin, co-twin unaffected), the probability of onset of major depression per month was predicted to be 0.5% and 6.2%, respectively, for those unexposed and exposed to a severe event. In those at highest genetic risk (monozygotic twin, co-twin affected), these probabilities were 1.1% and 14.6%, respectively. Linear regression analysis indicated significant Genotype by Environment interaction in the prediction of onset of major depression. Genetic factors influence the risk of onset of major depression in part by altering the sensitivity of individuals to the depression-inducing effect of stressful life events.
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              Critical Slowing Down as a Personalized Early Warning Signal for Depression.

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                Author and article information

                Contributors
                Journal
                Front Psychol
                Front Psychol
                Front. Psychol.
                Frontiers in Psychology
                Frontiers Media S.A.
                1664-1078
                02 November 2017
                2017
                : 8
                : 1908
                Affiliations
                [1] 1Department of Psychiatry and Psychology, Maastricht University Medical Centre , Maastricht, Netherlands
                [2] 2Department of Psychiatry, Yale School of Medicine , New Haven, CT, United States
                [3] 3University Psychiatric Centre KU Leuven , Leuven, Belgium
                [4] 4Centre of Human Genetics, University Hospitals Leuven, KU Leuven , Leuven, Belgium
                [5] 5Department of Obstetrics and Gynecology, Ghent University Hospitals, Ghent University , Ghent, Belgium
                [6] 6Department of Neurology, Ghent University Hospital, Ghent University , Ghent, Belgium
                [7] 7Faculty of Psychology and Educational Sciences, Open University of the Netherlands , Heerlen, Netherlands
                [8] 8Department of Psychiatry, Interdisciplinary Center Psychopathology and Emotion Regulation, University of Groningen, University Medical Center Groningen , Groningen, Netherlands
                [9] 9Department of Psychosis Studies, Institute of Psychiatry, King's Health Partners, King's College London , London, United Kingdom
                [10] 10Department of Psychiatry, Brain Centre Rudolf Magnus, University Medical Centre Utrecht , Utrecht, Netherlands
                Author notes

                Edited by: Pietro Cipresso, Istituto Auxologico Italiano (IRCCS), Italy

                Reviewed by: Yilun Shang, Tongji University, China; Tommaso Gili, Enrico Fermi Center, Italy

                *Correspondence: Laila Hasmi l.hasmi@ 123456maastrichtuniversity.nl

                This article was submitted to Quantitative Psychology and Measurement, a section of the journal Frontiers in Psychology

                Article
                10.3389/fpsyg.2017.01908
                5673657
                29163289
                9497f12c-b20c-4921-a029-5bb9282c8b44
                Copyright © 2017 Hasmi, Drukker, Guloksuz, Menne-Lothmann, Decoster, van Winkel, Collip, Delespaul, De Hert, Derom, Thiery, Jacobs, Rutten, Wichers and van Os.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 14 July 2017
                : 16 October 2017
                Page count
                Figures: 3, Tables: 5, Equations: 0, References: 49, Pages: 14, Words: 9370
                Funding
                Funded by: European Commission Seventh Framework Programme 10.13039/100011102
                Award ID: HEALTH-F2-2009-241909
                Categories
                Psychology
                Original Research

                Clinical Psychology & Psychiatry
                emotion dynamics,directed,weighted,network,time-series,genetic,psychopathology,childhood trauma

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