scholarly journals Emotion Regulation and Vulnerability to Depression: A Longitudinal Test of the Diathesis-Stress Model

2021 ◽  
Author(s):  
◽  
Michael Douglas Tooley

<p>Maladaptive emotion regulation is an established vulnerability marker for depression. Within a diathesis-stress framework individual differences in emotion regulation constitute sensitivity to stress, such that people who are less able to effectively regulate their emotions are more likely to become depressed when stress is encountered. Markers of maladaptive emotion regulation have been examined from affective, neurological, and cognitive perspectives and, for the most part, have been examined in independent lines of research. As such, the independent and interactive contributions of maladaptive emotion regulation markers are still unknown. The current thesis addresses this gap with a longitudinal study. Emotion regulation markers and depression were assessed at the outset of the study (time one) then life stress and depression were measured three months (time two) and twelve months (time three) later. Three trait measures of emotion regulation were assessed: spontaneous emotion regulation (as indexed by startle reactivity following negative images), frontal and parietal resting EEG asymmetries, and brooding rumination. All emotion regulation markers were found to be independent markers of vulnerability to depression. The emotion regulation markers measured at time one were then tested within a diathesis stress framework to predict stress sensitivity at time two. Poorer online regulation interacted with life stress to predict depression. That is, poor online regulators were sensitive to stress at three months, whereas good online regulators were not. Stress sensitivity was tested again at time three, twelve months after the initial assessment. At this time point frontal asymmetry, parietal asymmetry and life stress interacted to predict depression. When right parietal activity was low, rightward frontal asymmetries showed more sensitivity to stress. However, people with leftward asymmetries showed less stress sensitivity. Brooding predicted depression at three months but not at twelve months and did not interact with stress at either time point. The findings of this thesis show that, within the diathesis-stress framework, online regulation measures indicate short-term sensitivity to stress; however, EEG asymmetry measures show sensitivity to stress in the longer term.</p>

2021 ◽  
Author(s):  
◽  
Michael Douglas Tooley

<p>Maladaptive emotion regulation is an established vulnerability marker for depression. Within a diathesis-stress framework individual differences in emotion regulation constitute sensitivity to stress, such that people who are less able to effectively regulate their emotions are more likely to become depressed when stress is encountered. Markers of maladaptive emotion regulation have been examined from affective, neurological, and cognitive perspectives and, for the most part, have been examined in independent lines of research. As such, the independent and interactive contributions of maladaptive emotion regulation markers are still unknown. The current thesis addresses this gap with a longitudinal study. Emotion regulation markers and depression were assessed at the outset of the study (time one) then life stress and depression were measured three months (time two) and twelve months (time three) later. Three trait measures of emotion regulation were assessed: spontaneous emotion regulation (as indexed by startle reactivity following negative images), frontal and parietal resting EEG asymmetries, and brooding rumination. All emotion regulation markers were found to be independent markers of vulnerability to depression. The emotion regulation markers measured at time one were then tested within a diathesis stress framework to predict stress sensitivity at time two. Poorer online regulation interacted with life stress to predict depression. That is, poor online regulators were sensitive to stress at three months, whereas good online regulators were not. Stress sensitivity was tested again at time three, twelve months after the initial assessment. At this time point frontal asymmetry, parietal asymmetry and life stress interacted to predict depression. When right parietal activity was low, rightward frontal asymmetries showed more sensitivity to stress. However, people with leftward asymmetries showed less stress sensitivity. Brooding predicted depression at three months but not at twelve months and did not interact with stress at either time point. The findings of this thesis show that, within the diathesis-stress framework, online regulation measures indicate short-term sensitivity to stress; however, EEG asymmetry measures show sensitivity to stress in the longer term.</p>


2016 ◽  
Vol 5 (1) ◽  
pp. 150-157 ◽  
Author(s):  
Matthew A. Scult ◽  
Annchen R. Knodt ◽  
Johnna R. Swartz ◽  
Bartholomew D. Brigidi ◽  
Ahmad R. Hariri

Calculating math problems from memory may seem unrelated to everyday processing of emotions, but they have more in common than one might think. Prior research highlights the importance of the dorsolateral prefrontal cortex (dlPFC) in executive control, intentional emotion regulation, and experience of dysfunctional mood and anxiety. Although it has been hypothesized that emotion regulation may be related to “cold” (i.e., not emotion-related) executive control, this assertion has not been tested. We address this gap by providing evidence that greater dlPFC activity during cold executive control is associated with increased use of cognitive reappraisal to regulate emotions in everyday life. We then demonstrate that in the presence of increased life stress, increased dlPFC activity is associated with lower mood and anxiety symptoms and clinical diagnoses. Collectively, our results encourage ongoing efforts to understand prefrontal executive control as a possible intervention target for improving emotion regulation in mood and anxiety disorders.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Catherine Jensen Peña ◽  
Milo Smith ◽  
Aarthi Ramakrishnan ◽  
Hannah M. Cates ◽  
Rosemary C. Bagot ◽  
...  

Abstract Abuse, neglect, and other forms of early life stress (ELS) significantly increase risk for psychiatric disorders including depression. In this study, we show that ELS in a postnatal sensitive period increases sensitivity to adult stress in female mice, consistent with our earlier findings in male mice. We used RNA-sequencing in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of male and female mice to show that adult stress is distinctly represented in the brain’s transcriptome depending on ELS history. We identify: 1) biological pathways disrupted after ELS and associated with increased behavioral stress sensitivity, 2) putative transcriptional regulators of the effect of ELS on adult stress response, and 3) subsets of primed genes specifically associated with latent behavioral changes. We also provide transcriptomic evidence that ELS increases sensitivity to future stress through enhancement of known programs of cortical plasticity.


2020 ◽  
Vol 9 (2) ◽  
pp. 468 ◽  
Author(s):  
Clarissa Catale ◽  
Stephen Gironda ◽  
Luisa Lo Iacono ◽  
Valeria Carola

The putative effects of early-life stress (ELS) on later behavior and neurobiology have been widely investigated. Recently, microglia have been implicated in mediating some of the effects of ELS on behavior. In this review, findings from preclinical and clinical literature with a specific focus on microglial alterations induced by the exposure to ELS (i.e., exposure to behavioral stressors or environmental agents and infection) are summarized. These studies were utilized to interpret changes in developmental trajectories based on the time at which the stress occurred, as well as the paradigm used. ELS and microglial alterations were found to be associated with a wide array of deficits including cognitive performance, memory, reward processing, and processing of social stimuli. Four general conclusions emerged: (1) ELS interferes with microglial developmental programs, including their proliferation and death and their phagocytic activity; (2) this can affect neuronal and non-neuronal developmental processes, which are dynamic during development and for which microglial activity is instrumental; (3) the effects are extremely dependent on the time point at which the investigation is carried out; and (4) both pre- and postnatal ELS can prime microglial reactivity, indicating a long-lasting alteration, which has been implicated in behavioral abnormalities later in life.


2017 ◽  
Vol 31 (1) ◽  
pp. 85-103 ◽  
Author(s):  
Bertus F. Jeronimus ◽  
Harriëtte Riese ◽  
Albertine J. Oldehinkel ◽  
Johan Ormel

Adolescents’ temperamental frustration is a developmental precursor of adult neuroticism and psychopathology. Because the mechanisms that underlie the prospective association between adolescents’ high frustration and psychopathology (internalizing/externalizing) have not been studied extensively, we quantified three pathways: stress generation [mediation via selection/evocation of stressful life events (SLEs)], cross–sectional frustration–psychopathology overlap (‘carry–over’/common causes), and a direct (non–mediated) vulnerability effect of frustration, including moderation of SLE impact. Frustration and psychopathology were assessed at age 16 with the Early Adolescent Temperament Questionnaire and the Youth Self–Report. No gender differences in frustration were observed. At age 19, psychopathology was reassessed by using the Adult Self–Report, while occurrence of endogenous (self–generated) and exogenous (not self–generated) SLEs during the interval (ages 16–19) were ascertained with the Life Stress Interview, an investigator–based contextual–stressfulness rating procedure (N = 957). Half of the prospective effect of frustration on psychopathology was explained by baseline overlap, including effects of ‘carry–over’ and common causes, about 5% reflected stress generation (a ‘vicious’ cycle with the environment adolescents navigate and shape), and 45% reflected unmediated association: a direct vulnerability effect including stress sensitivity or moderation of SLE impact. After adjustment for their overlap, frustration predicted the development of externalizing but not internalizing symptoms. Copyright © 2016 European Association of Personality Psychology


2015 ◽  
Vol 27 (4pt1) ◽  
pp. 1007-1023 ◽  
Author(s):  
Ruth Feldman

AbstractElucidating the mechanisms by which infant birth conditions shape development across lengthy periods is critical for understanding typical and pathological development and for targeted early interventions. This study examined how newborns' regulatory capacities impact 10-year outcomes via the bidirectional influences of child emotion regulation (ER) and reciprocal parenting across early development. Guided by dynamic systems theory, 125 infants were tested at seven time points: birth, 3, 6, 12, and 24 months and 5 and 10 years. Initial regulatory conditions were measured by respiratory sinus arrhythmia (RSA; vagal tone) and neurobehavioral regulation (Brazelton, 1973) at birth. At each assessment between 3 months and 5 years, infant ER was microcoded from age-appropriate paradigms and mother–child reciprocity observed during social interactions. Four regulation-related outcomes were measured at 10 years: child RSA, empathy measured by mother–child conflict discussion and a lab paradigm, accident proneness, and behavior problems. An autoregressive cross-lagged structural model indicated that infant birth conditions impacted 10-year outcomes via three mechanisms. First, child ER and reciprocal parenting were individually stable across development and were each predicted by regulatory birth conditions, describing gradual maturation of ER and reciprocity over time. Second, better ER skills at one time point were related to greater reciprocity at the next time point and vice versa, and these cross-time effects defined a field of individual-context mutual influences that mediated the links between neonatal RSA and 10-year outcomes. Third, direct associations emerged between neonatal regulation and outcome, suggesting that birth conditions may establish a neurobiological milieu that promotes a more mature and resilient system. These mechanisms describe distinct “attractor” states that constrain the system's future options, emphasize the importance of defining behavior-based phenotypes of heterotypic continuity, and suggest that infants may shape their development by initiating unique cascades of individual-context bidirectional effects.


2021 ◽  
Author(s):  
Andrzej Sokołowski ◽  
Monika Folkierska-Żukowska ◽  
Katarzyna Jednoróg ◽  
Marek Wypych ◽  
Wojciech Ł. Dragan

AbstractStress may impact the ability to effectively regulate emotions. To study the impact of stressful experiences in early and recent life on emotion regulation, we examined the relationship between early life stress, recent stress, and brain activation during cognitive reappraisal. We investigated two regulation goals: the decrease and increase of emotional response to both negative and positive stimuli. Furthermore, two models of stress consequences were examined: the cumulative and match/mismatch models. A total of 83 participants (Mage = 21.66) took part in the study. There was an interaction between cumulative stress and stimuli valence in the cuneus, superior lateral occipital cortex, superior parietal lobule, supramarginal gyrus extending to superior temporal gyrus, and precentral gyrus extending to supplementary motor area. Interaction between mismatched stress index and stimuli valence was found in the left hippocampus, left insula extending to the orbitofrontal cortex and amygdala, and in a cluster including the anterior cingulate cortex, superior frontal gyrus, and frontal pole. Furthermore, there were differences between the effects of cumulative and mismatched stress indices on brain activation during reappraisal of positive but not negative stimuli. Results indicate that cumulative stress and match/mismatch approaches are both useful for explaining brain activation during reappraisal. This finding is important for our understanding of the multifaceted impact of stress on emotion regulation.


2019 ◽  
Author(s):  
Catherine Jensen Peña ◽  
Milo Smith ◽  
Aarthi Ramakrishnan ◽  
Hannah M. Cates ◽  
Rosemary C. Bagot ◽  
...  

ABSTRACTAbuse, neglect, and other forms of early life stress (ELS) significantly increase risk for psychiatric disorders including depression. In this study, we show that ELS in a postnatal sensitive period increases sensitivity to adult stress in female mice, consistent with our earlier findings in male mice. We used RNA-sequencing in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of male and female mice to show that adult stress is distinctly represented in the brain’s transcriptome depending on ELS history. We identify: 1) biological pathways disrupted after ELS and associated with increased behavioral stress sensitivity, 2) putative transcriptional regulators of the effect of ELS on adult stress response, and 3) subsets of primed genes specifically associated with latent behavioral changes. We also provide transcriptomic evidence that ELS increases sensitivity to future stress through enhancement of known programs of cortical plasticity.


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